In research, which will be published in the British Journal of Nutrition this week, a team led by Dr Jeremy Spencer of Reading University, found that champagne has the same health benefits as previously found in red wine.
It contains polyphenol antioxidants, which are believed to reduce the effects of cell-damaging free radicals in the body. In particular, these antioxidants slow down the removal of nitric oxide from the blood, lowering blood pressure and therefore reducing the risk of heart problems and strokes.
Related Articles
Skimmed milk cuts blood pressure research suggests
Income from property: home work
Aspirin 'can help prevent liver damage'
Sweaty music find could help develop new treatments
Drinking tea can reduce heart attack risk
Dr Spencer told a Sunday newspaper: "We have found that a couple of glasses a day has a beneficial effect on the walls of blood vessels – which suggests champagne has the potential to reduce strokes and heart disease.
"It is very exciting news."
And the benefits are not limited to alcoholic drinks. Dr Spencer has also found high levels of the antioxidant in cocoa beans meaning a mug of hot cocoa before bedtime is just as good, but, as he points out, "it doesn't seem as much fun somehow".
Cheaper champagne alternatives such as cava and Prosecco have also been found to contain the antioxidants.
The research was undertaken following a question mark over polyphenol levels in champagne. The antioxidant was known to be present in red wine and absent from white wine, but as champagne contains both red and white grapes there was uncertainty over polyphenol levels.
Champagne is made from a mixture of two black grape varieties, pinot noir and pinot meunier, and one white grape variety, chardonnay.

__________________________________________________

Pop the Champagne for Heart Health
Study finds link between sparkling wine and improved circulation

Posted:

Champagne producers have always touted that it's a wine worthy of daily consumption, not just for celebrations. And a study published in the Nov. 30 issue of the British Journal of Nutrition backs that up. The study, conducted by researchers at the school of chemistry, food and pharmacy at the University of Reading, with assistance from two biochemical and molecular biology centers in Reims, France, found that subjects who drank moderate amounts of Champagne daily appeared to show improved arterial function.

"This study into the effects of Champagne on the health of the circulatory system and the heart suggests that Champagne acts in a way more akin to red wine than to white wine and that these effects are due to polyphenols derived from both the red and white grape used in its production," said Jeremy P.E. Spencer, a researcher at the University who also coauthored earlier research that found Champagne protects brain cells from injury.

In the text, the authors point out that past studies have suggested a correlation between red wine consumption and lower incidence of cardiovascular disease but that Champagne has not been fully investigated for cardio-protective potential. To do just that, the researchers set up a randomized, placebo-controlled, crossover intervention trial, where subjects would drink moderate amounts of Champagne daily. They theorize that because Champagne is made from both white and red grapes, it may offer red wine’s cardiovascular benefits.

The volunteers, ages 20 to 65, were recruited from around Reading and cleared vigorous medical tests to ensure they were free of any chronic illnesses. Leading up to the study, the scientists suspected that certain plant-based chemicals in the subjects' diets may impact the results and asked participants to forgo polyphenol-rich products such as cocoa, coffee, tea and wine for two days prior to the experiment.

On the first day of the research, subjects drank 375 milliliters of Champagne. In the control group, the subjects drank a carbonated fruit-based beverage mixed in the lab with a similar 12 percent alcohol and an equivalent amount of ethanol, sugars, vitamins, minerals and acids. The only major difference in composition, Spencer explained, is that the control beverage did not contain polyphenols.

Regardless of what they were drinking, the volunteers were given 10 minutes to get it all down. Blood samples were then collected at regular intervals for eight hours, and urine was taken every eight hours for the following day.

In the blood samples, the researchers noted that levels of nitric oxide, a molecule that controls blood pressure, were elevated in the Champagne drinkers. Optimal nitric oxide levels should decrease the risk of blood clots forming and, therefore, the study concludes, this should equally decrease the likelihood of heart disease and strokes. Furthermore, metabolites of Champagne polyphenols were detected in the urine samples, indicating a decent rate of absorption into the blood.

The levels of nitric oxide in the blood and polyphenol metabolites in the urine were higher in the Champagne group when compared to the control groups. "Our research has shown that drinking around two glasses of Champagne can have beneficial effects on the way blood vessels function, in a similar way to that observed with red wine," said Spencer, in a statement. He stressed, however, that, "We always encourage a responsible approach to alcohol consumption."

Moderate Champagne consumption promotes an acute improvement in acute endothelial-independent vascular function in healthy human volunteers

David Vauzour¹, Emily J. Houseman¹, Trevor W. George², Giulia Corona¹, Roselyne Garnotel^3,4, Kim G. Jackson², Christelle Sellier³, Philippe Gillery^3,4, Orla B. Kennedy², Julie A. Lovegrove² and Jeremy P. E. Spencer^1,2*

¹Molecular Nutrition Group, School of Chemistry, Food and Pharmacy, University of Reading, Reading RG6 6AP, UK
²Hugh Sinclair Human Nutrition Group, School of Chemistry, Food and Pharmacy, University of Reading, Reading RG6 6AP, UK
³Laboratoire de Biochimie et Biologie Mole´culaire, UFR Me´decine, CNRS UMR 6237, IFR 53, 51 rue Cognacq-Jay, 51095 Reims, France
⁴Laboratoire de Biologie et de Recherche Pe´diatriques, CHU, 47 rue Cognacq-Jay, 51092 Reims, France

(Received 10 August 2009 – Revised 15 October 2009 – Accepted 19 October 2009)

Epidemiological studies have suggested an inverse correlation between red wine consumption and the incidence of CVD. However, Champagne wine has not been fully investigated for its cardioprotective potential. In order to assess whether acute and moderate Champagne wine consumption is capable of modulating vascular function, we performed a randomised, placebo-controlled, cross-over intervention trial. We show that consumption of Champagne wine, but not a control matched for alcohol, carbohydrate and fruit-derived acid content, induced an acute change in endothelium- independent vasodilatation at 4 and 8 h post-consumption. Although both Champagne wine and the control also induced an increase in endothelium-dependent vascular reactivity at 4 h, there was no significant difference between the vascular effects induced by Champagne or the control at any time point. These effects were accompanied by an acute decrease in the concentration of matrix metalloproteinase (MMP-9), a significant decrease in plasma levels of oxidising species and an increase in urinary excretion of a number of phenolic metabolites. In particular, the mean total excretion of hippuric acid, protocatechuic acid and isoferulic acid were all significantly greater following the Champagne wine intervention compared with the control intervention. Our data suggest that a daily moderate consumption of Champagne wine may improve vascular performance via the delivery of phenolic constituents capable of improving NO bioavailability and reducing matrix metalloproteinase activity.

Champagne wine intake: Endothelial-independent vascular function: Matrix metalloproteinase-9 activity: Cardiovascular disease

Epidemiological studies have suggested that there is an inverse correlation between the consumption of polyphenolrich foods and the prevention of CVD^(1,2). Moderate red wine intake has also been associated with a reduced coronary artery disease mortality^(3,4), which may be due to its ability to improve endothelial function⁽⁵⁾, induce an acute increase in endothelium-dependent flow-mediated dilatation^(6,7) and inhibit endothelin-1 synthesis^(8,9). These effects of red wine have been linked to both its alcohol content and to its high content of polyphenols, in particular flavonoids, hydroxycinnamates and phenolic acids⁽¹⁰⁾. Following consumption, nanomolar quantities of flavonoids and other polyphenols enter the circulation^(10,11) where they may act to improve NO bioavailability and/or inhibit endothelin-1^(12,13). In support of this, white wine, which has significantly lower concentration of polyphenols, induces significant reduced vascular effects^(14,15), although its cardioprotective effects have been reported^(16,17). In contrast to white wine, Champagne wine is relatively rich in polyphenols such as hydroxybenzoic acids, hydroxycinnamic acids (and their tartaric derivative esters), flavonoids, phenolic alcohols and phenolic aldehydes⁽¹⁸⁾. The increased levels of phenolics in Champagne wine derive predominantly from the two red grapes, Pinot Noir and Pinot Meunier, which are used in its production along with the white grape Chardonnay⁽¹⁹⁾. Moderate Champagne wine consumption has been shown to exert a number of effects in vivo, effecting peripheral serotonin and dopamine release⁽²⁰⁾ and increasing plasma vitamin A concentration⁽²¹⁾. Champagne wine polyphenols have also be shown to protect cells against injury induced by peroxynitrite⁽²²⁾, a physiologically relevant oxidising species which has been implicated in vascular wall pathology^(23,24). However, thus far, there have been no studies investigating its consumption and changes in endothelial function and thus cardiovascular risk. In the present study, we have performed a randomised, single-blind, controlled, cross-over design study in order to assess whether acute, moderate Champagne wine consumption is capable of modulating endothelial function in healthy human volunteers. We show that consumption of Champagne wine induces acute changes in endothelium-independent vasodilatation but not endothelium-dependent vasodilatation. These effects were accompanied by a change in the level of matrix metalloproteinase-9 (MMP-9), reductions in plasma levels of oxidants and with an increased urinary excretion of a number of phenolic metabolites. Together, our data suggest that moderate Champagne wine consumption may help to improve cardiovascular risk via its effects on the vasculature and that that these effects may be mediated by circulating Champagne wine-derived polyphenols.

Material and methods

Materials

Phenolic standards (caffeic acid, ferulic acid, homovanillyl alcohol, gallic acid, vanillic acid, p-hydrobenzoic acid, (+)- catechin, (-)-epicatechin, hydroxytyrosol, vanillin, hydroxyhippuric acid, p-coumaric acid, protocatechuic acid, sinapic acid, hydroferulic acid, 3,4-dihydroxyphenylacetic acid, tryptophol, resveratrol, quercetin, hippuric acid) and type H-1 b-glucuronidase from elix pomatia (EC 3.2.1.31) were all obtained from Sigma (Poole, Dorset, UK). Caftaric acid was obtained from Apin Chemicals Abingdon, Oxon, UK), homovanillic acid was obtained from Lancaster Synthesis Ltd (Heysham, Lancs, UK) and tyrosol and isoferulic acid were purchased from Extrasynthese (Lyon, France). Solvents were all of HPLC grade and were purchased from Fisher Scientific (Loughborough, Leics, UK). Ethyl acetate was purified by distillation on a Raschig column before use. The K2EDTA, serum separation tubes and heparin vacutainer tubes were obtained from BD Vacutainer (Oxford, Oxon, UK). Wallace Y-can cannulas were from 3S Healthcare (Enfield, London, UK).

Subjects

Healthy male and female subjects (n 15), aged between 20 and 65 years (mean age 39·5 (SEM 4·3) years) with a BMI of 18·9– 28·4 kg/m² (mean BMI 23·6 (SEM 0·7) kg/m²), were recruited from the University of Reading and surrounding area. Individuals with diabetes mellitus, any form of liver or gastrointestinal disorder, high blood pressure (>150/90 mm/Hg), anaemia, gall bladder problems, present illness, or those taking dietary supplements, consuming caffeine or aspirin, vigorous exercise (more than three times X 20 min per week), or alcohol consumption more than 120 g (women) and 168 g (men) per week were excluded from the study, along with pregnant or lactating females. Subjects were healthy, based on a medical questionnaire, and had normal concentrations of liver enzymes (aspartate aminotransferase, alanine aminotransferase and g-glutamyl transferase), normal Hb, packed cell volume and leucocyte counts and an absence of glucose and protein in urine.

Study design

The study was conducted according to the guidelines laid down in the Declaration of Helsinki and all procedures involving human subjects were approved by the University of Reading Research Ethics Committee (ref. 07/16). The study was also registered with the National Institutes of Health (NIH) randomised trial records held on the NIH Clinical- Trials.gov website (ref. NCT00937313) and with the Current Controlled Trials website (ref. ISRCTN38867650). Written informed consent was obtained from all subjects before the study started. Subjects refrained from consuming high-polyphenol foods for 48 h before the start of the study and for 32 h post-initiation. In particular, the following foods and beverages were excluded from volunteer diets: cocoa-containing products, coffee, tea and wine. The study was designed as a single-blind, randomised, cross-over intervention trial, where volunteers were asked to consume either 375 ml of Champagne wine (Chardonnay, Pinot Noir and Pinot Meunier; 12% alcohol) or a control matched for alcohol content, fruit sugars and acids (Table 1). The Champagne wine used in the study contained no vitamin C. Subjects were assessed for anthropometric measurements and provided a urine sample before baseline laser Doppler imaging with iontophoresis (LDI) measurements (detailed below). Subjects were then cannulated in the antecubital vein and one baseline blood sample was collected. Subjects were then randomly assigned to either the Champagne wine or control group and asked to consume the beverage within a 10 min period. Following a standardised breakfast, blood samples were collected at 15, 30, 45, 60, 120, 180, 240, 300, 360 and 480 min postconsumption and pooled urine samples were collected over 3 X 8 h periods. A standardised breakfast and lunch were consumed at 15 and 200 min post-beverage. LDI measurements were carried out at 120, 240, 360 and 480 min. Subjects also provided 24 h and 32 h blood and urine samples.

Table 1. Composition of Champagne wine and placebo
(Mean values and standard deviations)

Following a washout period of 28 d, volunteers returned to the unit to complete the second arm of the study where the procedure above was repeated.

Laser Doppler imaging with iontophoresis

In all cases, subjects were rested in the supine position for 30 min in a temperature-controlled environment (22–24°C) before LDI determination. Peripheral microvascular function was assessed using a validated technique which quantifies the vasodilator responses to 1% acetylcholine (endotheliumdependent vasodilatation) and 1% sodium nitroprusside (endothelial-independent vasodilatation), delivered transdermally using iontophoresis. This non-invasive in vivo method provides a robust surrogate marker of vascular function, as described previously^(25,26). For the vascular reactivity measurements, participants were requested to lie in a semirecumbent position with their right arm supported. A temperature probe and iontophoresis chambers were attached to the volar aspect of the forearm and freshly prepared solutions of acetylcholine chloride (2·5 ml; 1% (w/v) in 0·5% (w/v) NaCI solution; Sigma Aldrich, Poole, Dorset, UK) and
sodium nitroprusside (2·5 ml; 1% (w/v) in 0·5% (w/v) NaCI solution; Sigma Aldrich) were introduced into the anodal and cathodal chambers respectively. Following a basal measurement of skin perfusion, an incremental current was delivered progressively in 5µA steps (5, 10, 15 and 20µA) to yield a total charge (current X time) of 8000 coulombs during a 20 min measurement. A series of fifteen scans was performed as the current increased from 0 to 20 mA (with a further five scans performed following current termination) and skin perfusion, or erythrocyte flux, was measured using a laser Doppler imager (Moor Instruments Ltd, Axminster, Devon, UK). In all cases the within-day and between-day CV were less than 10 %, as previously reported⁽²⁷⁾.

Matrix metalloproteinase and tissue inhibitor of metalloproteinase analysis

MMP and tissue inhibitor of metalloproteinase (TIMP) were analysed by gelatine zymography and reverse zymography, respectively, as previously described⁽²⁸⁾. Briefly, for the detection of gelatinases in serum, SDS-PAGE was performed on gels containing 0·1% gelatine and 9% polyacrylamide. Samples (dilution 1/50), previously mixed with loading buffer (2% SDS and 0·1% bromophenol blue), were electrophoresed under non-reducing conditions. After electrophoresis, gels were washed in 2% Triton X-100 and immersed in buffer containing 50mM-2-amino-2-hydroxymethylpropane- 1,3-diol (Tris)-HCI (pH 7·6), 200mM-NaCI and 10mM-CaCI₂ for 18 h at 378C. The gels were stained with 0·5% Coomassie blue G-250 in acetic acid–methanol–water (1:4:5, by vol.) and de-stained in acetic acid–methanol– water (1:2:7, by vol.). The gelatinolytic activities appeared as clear bands against the blue background of gelatine. For the detection of TIMP in serum, SDS-PAGE was performed on gels containing 0·1% gelatine, 12% polyacrylamide and pro-MMP-2 (20 ng/ml). Samples (dilution 1/50), previously mixed with loading buffer (2% SDS and 0·1% bromophenol blue), were electrophoresed under non-reducing conditions. After electrophoresis, gels were washed in 2% Triton X-100 and immersed in buffer containing 50mM-Tris-HCIl (pH 7·6), 200mM-NaCl and 10mM-CaCl₂ for 18 h at 378C. The gels were stained with 0·5% Coomassie blue G-250 in acetic acid–methanol–water (1:4:5, by vol.) and de-stained in acetic acid–methanol–water (1:2:7, by vol.). Reverse zymography revealed inhibitory activity, which appeared as blue zones against a clear background, demonstrating inhibition of gelatine lysis in the gels. MMP-2, MMP-9, TIMP-1 and TIMP-2 concentrations in serum were quantified with human commercial ELISA kits (Amersham Biosciences) following the manufacturer’s instructions. Each sample was assayed in duplicate, and the values were within the linear portion of the standard curve.

HPLC analyses

Analysis of Champagne wine extracts for phenolic content were performed as previously described⁽²²⁾. Determination of the excreted urinary metabolites was carried out as follows: untreated urine samples were filtered through a 0·4µm membrane before HPLC analysis. For b-glucuronidase treatment, urine samples (1 ml) were acidified with 1·2 M-acetic acid (50µl) and mixed with ß-glucuronidase (230 mg/ml in 0·2 M-sodium acetate; pH 5) under Ar for 45 min at 378C. After addition of 1 M-HCl (40 µl), samples were extracted twice with ethyl acetate and centrifuged for 15 min at 5000 g. The combined organic layers were evaporated under N₂, re-dissolved by vortexing in 25% aqueous methanol (200µl), filtered (polytetrafluoroethylene (PTFE) membrane, 0·45µm; Millipore, Chandlers Ford, Hants, UK) and injected (50µl) onto an Agilent 1100 Series HPLC linked to a diode array detector. Sample separation was achieved using a C18 Nova Pak® column (250 X 4·6mm internal diameter; 5mm particle size), fitted with a guard column C18 NovaPak® (Waters Ltd, Elstree, Herts, UK). The mobile phase consisted of: A, aqueous methanol (5 %) þ 5M-HCl (0·1 %) and B, acetonitrile–methanol (1:1) þ 5 M-HCl (0·1 %) and was pumped through the column at 0·7 ml/min. Samples (50ml) were injected and separated using the following gradient system (min/% B): 0/5, 5/5, 40/50, 55/100, 59·9/100, 60/5 and the eluant was monitored by photodiode array detection at 254, 280, 320 and 370 nm, with spectra of products obtained over the 220–600 nm range. All data were analysed using ChemStation® software (Agilent Technologies, Inc., Santa Clara, CA, USA). Components were identified according to retention time, UV or visible spectra and spiking with commercially relevant standards when available.

Biochemical analysis

The blood samples collected in lithium–heparin tubes were spun (1700 g; 10 min; 4°C) immediately after collection. Samples were also collected in serum separation tubes (SST) and allowed to stand for 30 min before centrifugation (1300 g; 10 min; 21°C). All samples were sampled and frozen at - 80°C until analysis. All biochemical parameters were assayed on an ILAB 600 chemistry analyser (Instrumentation Laboratory, Warrington, Cheshire, UK) using enzymebased colorimetric tests supplied by Instrumentation Laboratory. The following parameters were determined in all samples: total cholesterol, LDL-cholesterol, HDL-cholesterol, glucose, TAG, uric acid, total bilirubin, albumin, C-reactive protein, aspartate aminotransferase, alanine aminotransferase and g-glutamyl transferase. Plasma total antioxidant capacity (TAC) was measured by using the TAC kit provided by Medicon SA (Gerakas, Greece) as reported previously⁽²⁹⁾. This assay is based on the competition of a parallel reaction, where the peroxyl-radical donor 2,2-azobis-(2-amidinopropane) dihydrochloride (ABAP) bleaches the carotenoid crocin. Antioxidants present in the sample then inhibit the bleaching by trapping formed radicals. The assay was performed at 37°C in the following steps: 2µl of sample, calibrator or control were mixed with 250µl of crocin reagent (R1) and incubated for 160 s. Subsequently, 125µl ABAP (R2) were added and the decrease in absorbance at 450 nm was measured 256 s later. Values of TAC were expressed as mmol/l of Trolox and corrected TAC values were calculated from TAC after subtraction of the interactions due to endogenous uric acid, bilirubin and albumin accounting for 0·11, 0·11 and 0·01 mmol/mg of the antioxidant capacity, respectively ^(29,30). Endothelin-1 was determined using ELISA kits obtained from R&D Systems (Abingdon, Oxon, UK). Total NO levels were assessed by using the Total NO/Nitrite/Nitrate assay kit (ref. KGE001) obtained from R&D Systems. Total NO (NO^-₂/NO^-₃) in serum/plasma ranged between 10 and 97µmol/l (mean 37 µmol/l; n 25). Before analysis, samples were deproteinised by using 10 000 Da molecular-weight cutoff filters (R&D Systems). Total oxidative capacity (TOC) was determined by a rapid enzymic in vitro diagnostic assay (POX-ACT) obtained from Tatzber KEG (Höflein at theDanube, Austria)⁽³¹⁾. This assay measures endogenous levels of peroxides, an indicator of either the production of prooxidative substances by the organism or an impaired uptake or consumption of antioxidants, using tetramethylbenzidine as the chromogen substrate. This assay is robust and provides intra- and inter-assay CV of 3·73 and 5·51 %, respectively.

Statistical analysis

Data were analysed using SPSS version 12.1 (SPSS, Inc., Chicago, IL, USA). Results are presented in the text and figures as mean values with their standard errors. Bonferroni tests for multiple comparisons and t tests were subsequently used to examine differences between individual treatments. All data were checked for normality and log-transformed where necessary before statistical analysis Values of P<0·05 were taken as significant.

Results

Assessment of vascular reactivity by laser Doppler imaging with iontophoresis

Consumption of both the Champagne wine (P=0·030) and the control (P=0·045) induced an increase in endotheliumdependent vascular reactivity at 4 h, as indicated by increases in skin erythrocyte flux in the presence of acetylcholine chloride (Fig. 1(a)). These increases in vascular reactivity returned to baseline by 8 h and there was no significant difference between the vascular effects induced by Champagne wine or the control at any time point. Endothelium-independent vasodilatation (skin erythrocyte flux following iontophoresiswith sodium nitroprusside) was found to be significantly increased at 4 and 8 h Champagne wine consumption (P=0·045 and P=0·037, respectively) and a close to linear correlation was found between treatment and time (P=0·057). In contrast, the alcohol-matched control did not induce endothelium-independent changes in vascular reactivity. Furthermore, there was a significantly greater degree of endothelium-independent vasodilatation observed following Champagne wine intervention relative to placebo intervention at 4, 6 and 8 h (P=0·013, P=0·034 and P=0·031, respectively).

Fig. 1. Response of forearm skin erythrocyte flux v. baseline, following the iontophoresis of (a) acetylcholine or (b) sodium nitroprusside. (—•—), Champagne; (- -.- -), placebo. Values are means, with standard errors represented by vertical lines. The vasodilatation to sodium nitroprusside was ignificantly higher in the Champagne wine group than the placebo group (P<,0·05). * Mean value was significantly different from that at baseline (0 h) (P<0·05). † Mean value was significantly different from that following placebo intake (P<0·05).

Urinary excretion of polyphenols

The major phenolic derivatives indentified in urine were hippuric acid, protocatechuic acid, isoferulic acid, homovanillic acid, homovanillyl alcohol and 3,4-dihydroxyphenylacetic acid (Fig. 2). All of these compounds were present in baseline urine samples and all, with the exception of isoferulic acid, increased significantly over time following intervention with either Champagne wine or the alcohol control (Fig. 2). However, the mean total excretion of hippuric acid (Champagne wine, 159·30 (SEM 29·3) mg; control, 100·70 (SEM 20·8) mg; P<0·001), protocatechuic acid (Champagne wine, 10·60 (SEM 1·30) mg; control, 7·17 (SEM 1·56) mg; P<0·05) and isoferulic acid (Champagne wine, 2·04 (SEM 0·84) mg; control, 0·24 (SEM 0·39) mg; P<0·001) were all significantly greater following the Champagne wine intervention compared with the control intervention. More specifically, hippuric acid excretion (Fig. 2(a)) was significantly higher at 8 h (P=0·032) and 24 h (P=0·036) and protocatechuic acid excretion (Fig. 2(b)) was greater at 24 h (P=0·038) post-Champagne wine intervention compared with control. Isoferulic acid, which was present at very low concentration in baseline urine, increased significantly only following Champagne wine consumption and was significantly different from control at 24 h (P=0·039) and 32 h (P=0·011) post-intervention (Fig. 2(c)). Although there was a tendency for excretion to be increased following Champagne wine intervention, there were no significant differences in the mean total excretion of homovanillic acid (Champagne wine, 8·04 (SEM 1·51) mg; control, 7·07 (SEM 1·73) mg), homovanillyl alcohol (Champagne wine, 11·35 (SEM 1·91) mg; control, 9·15 (SEM 1·89)) or 3,4-dihydroxyphenylacetic acid (Champagne wine, 18·74 (SEM 3·58) mg; control, 21·34 (SEM 4·98) mg).

Biochemical markers

A significant increase in TAG concentrations was observed 6 h post-consumption of both Champagne wine and control, although there was no significant difference in the magnitude of change induced by the two interventions (Table 2). No significant changes in glucose, total cholesterol, HDL-cholesterol or LDL-cholesterol were observed post-Champagne wine or control consumption. All endothelial markers (endothelin-1, total NO/nitrite/nitrate) revealed values within a normal healthy range but did not change significantly following either intervention (Table 2). Liver enzyme levels (alanine aminotransferase, aspartate aminotransferase, g-glutamyl transferase) did not show any statistical changes in response to either intervention. All biochemical markers were within the expected healthy range.

Oxidative status and inflammatory markers

Intervention with both the control and Champagne wine led to increases in ‘total oxidant capacity’ (TOC) over the 6 h period immediately post-consumption, reflecting increases in endogenous peroxide production (P<0·001; Fig. 3).

 

In general, this increase in TOC was greater following the control intervention and was found to be significantly lower in the Champagne wine group at 6 h post-intervention (11% reduction relative to placebo; P<0·01) (Fig. 3). In contrast, there were no differences in ‘total antioxidant’ levels (corrected TAC) following either intervention (Table 2). Furthermore, there were no significant alterations in serum levels of C-reactive protein following either intervention.

Matrix metalloproteinase and tissue inhibitor of metalloproteinase levels

Gelatin–zymography analysis and ELISA revealed a stable concentration of MMP-2 at 1, 6 and 23 h post-intervention with Champagne wine and control (Fig. 4). In contrast, MMP-9 significantly decreased 1 h post-Champagne wine consumption (38·1 (SEM 6·3) %; P<0·05) but not following the control intervention (Fig. 4(a) and (d)). No significant modifications in the concentrations of TIMP-1 and TIMP-2 were observed (Fig. 4(b), (e) and (f)).

Discussion

Many epidemiological studies have suggested that a daily and moderate consumption of red wine is associated with a lower incidence of CVD^{(32 – 34)}. In agreement with this, previous studies have indicated that red wine consumption significantly improves enthothelial function⁽⁸) and that these effects can be, in part, attributed to its polyphenol content⁽³⁵⁾. Many of the effects of red wine are compatible with the action of wine-derived polyphenols on endothelium-derived NO production, implying that NO might be a mediator for their vascular actions^(36,37). Indeed, a rapid activation of endothelial NO synthase and endothelium-dependent vasodilatation has been reported for grape-derived polyphenols in vitro⁽³⁸⁾ and a single dose of red wine has been shown to increase NO production⁽³⁹⁾ and endothelium-dependent dilation^(40,41) in healthy volunteers. There is also evidence that white wine and Cava (sparkling white wine) may exert vascular actions. It has been suggested that such effects may result from the synergistic actions of polyphenols and other phenolic constituents on LDL oxidation and platelet function^{(42 – 44)}. In the present study, we show that Champagne wine consumption is capable of inducing acute vascular effects and in modifying levels of specific vascular active components. The consumption of either Champagne wine or the alcohol control induced a rapid increase in endothelium-dependent vasodilatation, which returned to basal levels after 8 h. These observations are in agreement with previous studies which indicate that moderate alcohol is capable of inducing an acute increase in blood flow in an endothelium-dependent manner^{(6,7,40,41,45)}. However, we found that only the Champagne wine intervention was capable of significantly inducing an increase in endothelium-independent vasodilatation, which was maintained up to 8 h post-consumption. These data suggest that moderate Champagne wine consumption may enhance microvascular blood flow for a sustained period, through maintenance of local NO levels, in this case delivered via iontophoresis. Our data also suggest that this effect may be mediated by absorbed Champagne wine polyphenols, the metabolites of which (hippuric acid, isoferulic acid and protocatechuic acid) were detected in urine following
Champagne wine ingestion. These metabolites are known to derive from the bacterial metabolism of caffeic acid and other hydroxycinnamates in the large intestine⁽⁴⁶⁾. Whilst urinary hippuric acid may derive from aromatic amino acids, its increased excretion following Champagne wine ingestion indicates that absorption and metabolism of Champagne wine phenolic compounds, such as caffeic acid, had occurred post-consumption⁽⁴⁶⁾. In support of this, the increased excretion of isoferulic acid after Champagne wine consumption is a specific biomarker of caffeic acid absorption, as this metabolites is only derived from the 4-methoxylation of caffeic acid by catechol-O-methyltransferase⁽⁴⁷⁾ before or after its absorption⁽⁴⁶⁾. Furthermore, the majority of urinary isoferulic acid has been shown to result from the cleavage of the caffeoyl quinic acid derivative of caffeic acid^(10,48). Protocatechuic acid, which also increased in response to Champagne wine intervention, has previously been detected in human plasma following red wine consumption(49) and has been identified as the urinary product of hydroxycinnamate ingestion from various food sources^(50,51).

 

The presence of such metabolites in urine between 6 and 32 h suggests that caffeic acid and other phenolic metabolites are absorbed into the circulation following Champagne wine consumption. These phenolic metabolites may affect vascular function by improving local NO bioavailability by two potential mechanisms. First, they may increase the local half-life of NOz via reaction with reactive oxygen species, such as superoxide^{(52 – 54)}. In support of this, we observed a significant reduction in the ‘total oxidant capacity’ following Champagne wine intake, indicating that Champagne wine intervention leads to a reduction in plasma oxidant levels relative to control. Second, phenolic metabolites, such as those excreted post-Champagne wine consumption, may mimic NADPH oxidase inhibitors^{(55 – 57)}, such as apocynin (4'-hydroxy-3'-methoxyacetophenone), thereby reducing the cellular production of superoxide and increasing the half-life of NO, without any change in the rate of NO synthesis⁽⁵⁶⁾. Indeed, previous studies have shown that the presence of an aromatic vicinal hydroxy-methoxy arrangement is highly effective in defining NADPH oxidase inhibition^(56,57). Champagne wine phenolics such as tyrosol, hydroxytyrosol, ferulic acid and homovanillic alcohol have been shown to outcompete apocynin with respect to its inhibitory potency⁽⁵⁷⁾. The combined inhibition of NADPH oxidase and the scavenging of reactive oxygen species by phenolic metabolites would be expected to affect local NO concentrations without influencing global endothelial NO production. Such effects may influence blood pressure, something which is supported by previous data showing that a low-molecular-weight fraction (1 kDa) of Champagne wine induces an anti-hypertensive effect in animals⁽⁵⁸⁾rs such as NG-methyl-L-arginine (L-NMMA) or methylene blue⁽⁵⁹⁾. This suggests that the vascular effects induced by this phenolic may be mediated by the inhibition of Ca²⁺ channels and/or the blockage of the protein kinase C-mediated contractile mechanism, as has been observed for caffeic acid phenyl ester and sodium ferulate, respectively^(60,61). Further investigation is necessary to unravel the precise mechanism by which Champagne wine phenolics modulate endothelium-independent vasorelaxation in vivo. The Champagne wine intervention also had a potentially beneficial effect on the vascular system in its ability to inhibit MMP-9. MMP and their specific tissue inhibitors (TIMP) play an important role in the physiological maintenance of the extracellular matrix and the pathogenesis of vascular disease^(62,63). For example, the over-expression of MMP-9 has been reported in atherosclerotic plaques⁽⁶⁴⁾ and has been linked with plaque rupture through its capacity to thin the protecting fibrous cap of the plaque^(65,66). Individual red wine phenolics have been shown to inhibit gelatinase expression and/or activity⁽⁶⁷⁾. A transient inhibition of MMP-9 by Champagne wine phenolics could influence type IV collagen degradation and therefore improve basement membrane structural integrity. Although unlikely to have long-term implications on the vascular system, this acute inhibition of MMP-9 appears to be consistent with our other observations, as the ability of Champagne wine phenolics to reduce plasma oxidant formation would be expected to inhibit peroxynitrite formation, an oxidant known to activate MMP-9. Its effects on endothelial-independent vascular reactivity may indicate that Champagne wine has the potential to improve ‘reactivity’ in the cutaneous microvasculature (arterioles, capillaries and venules). If so, it could reduce stiffening of the conduit arteries and a decline in arterial compliance, something which is observed with ageing, in hypertensive patients, in diabetics and those with cardio- and cerebrovascular disease⁽⁶⁸⁾. Our findings may have wider significance in that attenuated cutaneous microvascular responses in heart transplant patients are paralleled by reduced responsiveness of coronary blood vessels⁽⁶⁹⁾. As such, our data suggest that moderate Champagne wine consumption may improve microvasculature blood flow and therefore vascular responsiveness generally. Further investigation will be necessary to determine whether acute, or indeed chronic, intake of Champagne has the potential to reduce CVD risk through its effects on microvascular responsiveness.

Acknowledgements

The authors wish to thank Ms Jan Luff, Ms Sofia Moran and Mr Anestis Dougkas for help with subject recruitment and study days. The authors are funded by the Biotechnology and Biological Sciences Research Council (BB/F008953/1; BB/E023185/1; BB/G005702/1).
J. P. E. S., D. V. and J. A. L. conceived of and designed the study. Whilst all authors played a role in data interpretation, the data were obtained as follows: E. J. H. and K. G. J, biochemical parameters; T. W. G. and E. J. H., LDI data; R. G., C. S. and P. G., MMP data. All authors were involved in manuscript preparation and read and approved the findings of the study. J. P. E. S. prepared the final manuscript.
The authors have no conflict of interest to disclose.

References

1. Hertog MG, Kromhout D, Aravanis C, et al. (1995) Flavonoid intake and long-term risk of coronary heart disease and cancer in the Seven Countries Study. Arch Intern Med 155, 381–386. Champagne intake promotes vascular function 9		36. Andriambeloson E, Magnier C, Haan-Archipoff G, et al. (1998) Natural dietary polyphenolic compounds cause endotheliumdependent vasorelaxation in rat thoracic aorta. J Nutr 128, 2324–2333.
2. Lampe JW (1999) Health effects of vegetables and fruit: assessing mechanisms of action in human experimental studies. Am J Clin Nutr 70, Suppl. 3, 475S–490S.		37. Flesch M, Schwarz A & Bohm M (1998) Effects of red and white wine on endothelium-dependent vasorelaxation of rat aorta and human coronary arteries. Am J Physiol 275, H1183–H1190.
3. Gronbaek M, Becker U, Johansen D, et al. (2000) Type of alcohol consumed and mortality from all causes, coronary heart disease, and cancer. Ann Intern Med 133, 411–419.		38. Anselm E, Chataigneau M, Ndiaye M, et al. (2007) Grape juice causes endothelium-dependent relaxation via a redox-sensitive Src- and Akt-dependent activation of eNOS. Cardiovasc Res 73, 404–413.
4. Klatsky AL, Friedman GD, Armstrong MA, et al. (2003) Wine, liquor, beer, and mortality. Am J Epidemiol 158, 585–595.		39. Matsuo S, Nakamura Y, Takahashi M, et al. (2001) Effect of red wine and ethanol on production of nitric oxide in healthy subjects. Am J Cardiol 87, 1029–1031.
5. Szmitko PE & Verma S (2005) Antiatherogenic potential of red wine: clinician update. Am J Physiol Heart Circ Physiol 288, H2023–H2030.		40. Vlachopoulos C, Tsekoura D, Tsiamis E, et al. (2003) Effect of alcohol on endothelial function in healthy subjects. Vasc Med 8, 263–265.
6. Agewall S, Wright S, Doughty RN, et al. (2000) Does a glass of red wine improve endothelial function? Eur Heart J 21, 74–78.		41. Bau PF, Bau CH, Naujorks AA, et al. (2005) Early and late effects of alcohol ingestion on blood pressure and endothelial function. Alcohol 37, 53–58.
7. Hashimoto M, Kim S, Eto M, et al. (2001) Effect of acute intake of red wine on flow-mediated vasodilatation of the brachial artery. Am J Cardiol 88, 1457–1460.		42. Natella F, Nardini M, Belelli F, et al. (2008) Effect of coffee drinking on platelets: inhibition of aggregation and phenols incorporation. Br J Nutr 100, 1276–1282.
8. Fitzpatrick DF, Hirschfield SL & Coffey RG (1993) Endothelium- dependent vasorelaxing activity of wine and other grape products. Am J Physiol 265, H774–H778.		43. Natella F, Nardini M, Belelli F, et al. (2007) Coffee drinking induces incorporation of phenolic acids into LDL and increases the resistance of LDL to ex vivo oxidation in humans. Am J Clin Nutr 86, 604–609.
9. Corder R, Douthwaite JA, Lees DM, et al. (2001) Endothelin-1 synthesis reduced by red wine. Nature 414, 863–864.		44. Pignatelli P, Ghiselli A, Buchetti B, et al. (2006) Polyphenols synergistically inhibit oxidative stress in subjects given red and white wine. Atherosclerosis 188, 77–83. 10 D. Vauzour et al.
10. Scalbert A & Williamson G (2000) Dietary intake and bioavailability of polyphenols. J Nutr 130, Suppl. 8S, 2073S–2085S.		45. Tawakol A, Omland T & Creager MA (2004) Direct effect of ethanol on human vascular function. Am J Physiol Heart Circ Physiol 286, H2468–H2473.
11. Spencer JP, Abd El Mohsen MM, Minihane AM, et al. (2008) Biomarkers of the intake of dietary polyphenols: strengths, limitations and application in nutrition research. Br J Nutr 99, 12–22.		46. Rechner AR, Spencer JP, Kuhnle G, et al. (2001) Novel biomarkers of the metabolism of caffeic acid derivatives in vivo. Free Radic Biol Med 30, 1213–1222.
12. Loke WM, Hodgson JM, Proudfoot JM, et al. (2008) Pure dietary flavonoids quercetin and (2)-epicatechin augment nitric oxide products and reduce endothelin-1 acutely in healthy men. Am J Clin Nutr 88, 1018–1025.		47. Mannisto PT & Kaakkola S (1999) Catechol-O-methyltransferase (COMT): biochemistry, molecular biology, pharmacology, and clinical efficacy of the new selective COMT inhibitors. Pharmacol Rev 51, 593–628.
13. Stoclet JC, Chataigneau T, Ndiaye M, et al. (2004) Vascular protection by dietary polyphenols. Eur J Pharmacol 500, 299–313.		48. Rechner AR, Kuhnle G, Bremner P, et al. (2002) The metabolic fate of dietary polyphenols in humans. Free Radic Biol Med 33, 220–235.
14. Shimada K, Watanabe H, Hosoda K, et al. (1999) Effect of red wine on coronary flow-velocity reserve. Lancet 354, 1002.		49. Caccetta RA, Croft KD, Beilin LJ, et al. (2000) Ingestion of red wine significantly increases plasma phenolic acid concentrations but does not acutely affect ex vivo lipoprotein oxidizability. Am J Clin Nutr 71, 67–74.
15. van Velden DP, Mansvelt EP, Fourie E, et al. (2002) The cardioprotective effect of wine on human blood chemistry. Ann N Y Acad Sci 957, 337–340.		50. Choudhury R, Srai SK, Debnam E, et al. (1999) Urinary excretion of hydroxycinnamates and flavonoids after oral and intravenous administration. Free Radic Biol Med 27, 278–286.
16. Cui J, Tosaki A, Cordis GA, et al. (2002) Cardioprotective abilities of white wine. Ann N Y Acad Sci 957, 308–316.		51. Olthof MR, Hollman PC, Buijsman MN, et al. (2003) Chlorogenic acid, quercetin-3-rutinoside and black tea phenols are extensively metabolized in humans. J Nutr 133, 1806–1814.
17. Dudley JI, Lekli I, Mukherjee S, et al. (2008) Does white wine qualify for French paradox? Comparison of the cardioprotective effects of red and white wines and their constituents: resveratrol, tyrosol, and hydroxytyrosol. J Agric Food Chem 56, 9362–9373.		52. Klotz LO & Sies H (2003) Defenses against peroxynitrite: selenocompounds and flavonoids. Toxicol Lett 140–141, 125–132.
18. Chamkha M, Cathala B, Cheynier V, et al. (2003) Phenolic composition of champagnes from Chardonnay and Pinot Noir vintages. J Agric Food Chem 51, 3179–3184.		53. Koppenol WH (1998) The basic chemistry of nitrogen monoxide and peroxynitrite. Free Radic Biol Med 25, 385–391.
19. Constant J (1997) Alcohol, ischemic heart disease, and the French paradox. Clin Cardiol 20, 420–424.		54. Radi R, Peluffo G, Alvarez MN, et al. (2001) Unraveling peroxynitrite formation in biological systems. Free Radic Biol Med 30, 463–488.
20. Boyer JC, Bancel E, Fabbro Perray P, et al. (2004) Effect of Champagne compared to still white wine on peripheral neurotransmitter concentrations. Int J Vitam Nutr Res 74, 264–271.		55. Halliwell B (1996) Antioxidants in human health and disease. Annu Rev Nutr 16, 33–50.
21. Cartron E, Fouret G, Carbonneau MA, et al. (2003) Red-wine beneficial long-term effect on lipids but not on antioxidant characteristics in plasma in a study comparing three types of wine – description of two O-methylated derivatives of gallic acid in humans. Free Radic Res 37, 1021–1035.		56. Schewe T, Steffen Y & Sies H (2008) How do dietary flavanols improve vascular function? A position paper. Arch Biochem Biophys 476, 102–106.
22. Vauzour D, Vafeiadou K, Corona G, et al. (2007) Champagne wine polyphenols protect primary cortical neurons against peroxynitrite- induced injury. J Agric Food Chem 55, 2854–2860.		57. Steffen Y, Schewe T & Sies H (2007) (2)-Epicatechin elevates nitric oxide in endothelial cells via inhibition of NADPH oxidase. Biochem Biophys Res Commun 359, 828–833.
23. van der Loo B, Labugger R, Skepper JN, et al. (2000) Enhanced peroxynitrite formation is associated with vascular aging. J Exp Med 192, 1731–1744.		58. Perrot L, Dukic S, Charpentier M, et al. (2003) Antihypertensive effect of a low molecular weight fraction (1 kDa) of champagne wine in spontaneously hypertensive rats. In Oenologie, pp. 688–691 [A Lonvaud-Funel, G Revel and P Darriet, editors]. Paris: Tec and Doc.
24. Xu S, Ying J, Jiang B, et al. (2006) Detection of sequencespecific tyrosine nitration of manganese SOD and SERCA in cardiovascular disease and aging. Am J Physiol Heart Circ Physiol 290, H2220–H2227.		59. Benkhalti F, Legssyer A, Gomez P, et al. (2003) Effects of virgin olive oil phenolic compounds on LDL oxidation and vasorelaxation activity. Therapie 58, 133–137.
25. Armah CK, Jackson KG, Doman I, et al. (2008) Fish oil fatty acids improve postprandial vascular reactivity in healthy men. Clin Sci (Lond) 114, 679–686.		60. Chen GP, Ye Y, Li L, et al. (2009) Endothelium-independent vasorelaxant effect of sodium ferulate on rat thoracic aorta. Life Sci 84, 81–88.
26. Ferrell WR, Ramsay JE, Brooks N, et al. (2002) Elimination of electrically induced iontophoretic artefacts: implications for non-invasive assessment of peripheral microvascular function. J Vasc Res 39, 447–455.		61. Cicala C, Morello S, Iorio C, et al. (2003) Vascular effects of caffeic acid phenethyl ester (CAPE) on isolated rat thoracic aorta. Life Sci 73, 73–80.
27. Ramsay JE, Ferrell WR, Greer IA, et al. (2002) Factors critical to iontophoretic assessment of vascular reactivity: implications for clinical studies of endothelial dysfunction. J Cardiovasc Pharmacol 39, 9–17.		62. Li YY, Feldman AM, Sun Y, et al. (1998) Differential expression of tissue inhibitors of metalloproteinases in the failing human heart. Circulation 98, 1728–1734.
28. Buache E, Garnotel R, Aubert D, et al. (2007) Reduced secretion and expression of gelatinase profile in Toxoplasma gondii-infected human monocytic cells. Biochem Biophys Res Commun 359, 298–303.		63. Visse R & Nagase H (2003) Matrix metalloproteinases and tissue inhibitors of metalloproteinases: structure, function, and biochemistry. Circ Res 92, 827–839.
29. Kampa M, Nistikaki A, Tsaousis V, et al. (2002) A new automated method for the determination of the total antioxidant capacity (TAC) of human plasma, based on the crocin bleaching assay. BMC Clin Pathol 2, 3.		64. Galis ZS, Sukhova GK, Lark MW, et al. (1994) Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest 94, 2493–2503.
30. Malliaraki N, Mpliamplias D, Kampa M, et al. (2003) Total and corrected antioxidant capacity in hemodialyzed patients. BMC Nephrol 4, 4.		65. Libby P, Schoenbeck U, Mach F, et al. (1998) Current concepts in cardiovascular pathology: the role of LDL cholesterol in plaque rupture and stabilization. Am J Med 104, 14S–18S.
31. Tatzber F, Griebenow S, Wonisch W, et al. (2003) Dual method for the determination of peroxidase activity and total peroxidesiodide leads to a significant increase of peroxidase activity in human sera. Anal Biochem 316, 147–153.		66. Loftus IM, Naylor AR, Bell PR, et al. (2002) Matrix metalloproteinases and atherosclerotic plaque instability. Br J Surg 89, 680–694.
32. Klatsky AL, Armstrong MA & Friedman GD (1992) Alcohol and mortality. Ann Intern Med 117, 646–654.		67. Dell’Agli M, Canavesi M, Galli G, et al. (2005) Dietary polyphenols and regulation of gelatinase expression and activity. Thromb Haemost 93, 751–760.
33. Renaud S & de Lorgeril M (1992) Wine, alcohol, platelets, and the French paradox for coronary heart disease. Lancet 339, 1523–1526.		68. Asmar RG, Pannier B, Santoni JP, et al. (1988) Reversion of cardiac hypertrophy and reduced arterial compliance after converting enzyme inhibition in essential hypertension. Circulation 78, 941–950.
34. St Leger AS, Cochrane AL & Moore F (1979) Factors associated with cardiac mortality in developed countries with particular reference to the consumption of wine. Lancet i, 1017–1020.		69. Andreassen AK, Kvernebo K, Jorgensen B, et al. (1998) Exercise capacity in heart transplant recipients: relation to impaired endothelium-dependent vasodilation of the peripheral microcirculation. Am Heart J 136, 320–328.
35. Dell’ Agli M, Busciala A & Bosisio E (2004) Vascular effects of wine polyphenols. Cardiovasc Res 63, 593–602.

__________________________________________________

 

Les vertus d'une consommation modérée de vin rouge sont connues depuis maintenant plusieurs années.
Mais qu'en est-il du champagne, roi des vins?
Renferme-t-il les mêmes bienfaits, n'a-t-il aucun intérêt nutritionnel ou,
au contraire, confère-t-il davantage de bénéfices pour la santé que le vin rouge?

 

Avec les fêtes, il n'est pas rare de boire une petite flûte de champagne. Or, il semble qu'une consommation modérée de ce breuvage confère, au même titre que le vin rouge, des bénéfices sur le plan cardiovasculaire mais également au niveau cérébral. Un vin blanc pas comme les autres Les vins blancs contiennent généralement peu de polyphénols par rapport aux vins rouges. Toutefois, il semble que les vins de Champagne ne soient pas des vins blancs comme les autres. Des études menées sur les champagnes blancs ont en effet démontré que ces derniers contenaient des quantités relativement élevées d'acides phénoliques, composés pouvant exercer un effet protecteur au niveau cellulaire in vivo. Une autre étude a également investigué les effets neuroprotecteurs d'extraits de champagne et des composés phénoliques individuels présents dans ces extraits contre les lésions induites par les peroxynitrites. Les résultats ont soulevé le fait que les extraits organiques et aqueux de vin de Champagne présentaient une puissante activité neuroprotectrice contre les lésions induites par les peroxynitrites à de faibles concentrations (0,1 pg/ml). Cette protection semble être due en partie à l'action des différents composants présents dans les extraits organiques tels que le tyrosol, l'acide caféique et l'acide gallique. Ces composés phénoliques sont en effet connus pour avoir des propriétés neuroprotectrices à des concentrations comprises entre 0,1 et 10 μM. Ces données suggèrent donc que les polyphénols présents dans le champagne pourraient induire un effet neuroprotecteur contre les lésions oxydatives neuronales. Bon pour le coeur Tous les professionnels de la santé le savent, il existe une corrélation inverse entre la consommation modérée de vin rouge (un à deux verres par jour) et l'incidence des maladies cardiovasculaires. Mais ce que l'on sait moins, c'est que les mêmes effets se retrouvent avec la consommation de champagne. Afin d'évaluer si une consommation modérée et aiguë de champagne permettait de moduler la fonction vasculaire, des chercheurs anglais ont mené il y a peu une étude interventionnelle randomisée, contrôlée contre placebo. Lors de cet essai, les scientifiques ont montré que la consommation de vin de Champagne induisait un changement aigu dans la vasodilatation endothélium-indépendante après quatre et huit heures suivant son ingestion. Ce n'était pas le cas pour la boisson utilisée dans le groupe témoin, bien que cette dernière soit similaire au champagne au niveau de la teneur en alcool, en glucides et en acides organiques. Outre ces effets, les auteurs ont également observé une baisse aiguë de la concentration en métalloprotéinases de la matrice (MMP-9), une diminution significative des concentrations plasmatiques d'espèces oxydantes et une augmentation de l'excrétion urinaire d'un certain nombre de métabolites phénoliques. L'excrétion totale moyenne de l'acide hippurique, de l'acide protocatéchique et de l'acide isoférulique était effectivement plus élevée après consommation de vin de Champagne par rapport à l'ingestion de la boisson contrôle. Ces données suggèrent donc qu'une consommation quotidienne modérée de vin de Champagne pourrait améliorer sensiblement les performances vasculaires. Alexandre Dereinne Références: Vauzour D, Vafeiadou K, Corona G et al. Champagne wine polyphenols protect primary cortical neurons against peroxynitrite-induced injury. J Agric Food Chem. 2007 Apr 18;55(8):2854-60. Epub 2007 Mar 24. Consulter la référence Vauzour D, Houseman EJ, George TW et al. Moderate Champagne consumption promotes an acute improvement in acute endothelial-independent vascular function in healthy human volunteers. Br J Nutr. 2010 Apr;103(8):1168-78. Epub 2009 Nov 30.