Biomedical subjects

R Andriantsitohaina

Publications and source records attributed to R Andriantsitohaina.

At least 19 recordsLinked to original sources

PubMed2006

Anti-proliferative effect of Euphorbia stenoclada in human airway smooth muscle cells in culture.

The ethanolic extract of a Malagasy species Euphorbia stenoclada (ES) (Euphorbiaceae), traditionally used as a herbal remedy against asthma and acute bronchitis, was tested to evaluate possible anti-proliferative activity on human airway smooth muscle cells (HASMC). The ES ethanolic extract totally abolished the interleukin-1beta (IL-1beta) induced proliferation of HASMC (IC(50)=0.73+/-0.08 microg/mL). No cytotoxic effect was observed up to 20 microg/mL. A bioassay-guided fractionation of the ethanolic extract was performed by reversed-phase (RP) flash chromatography, giving five fractions (FA to FE) where fraction FE was the only active one (IC(50)=0.38+/-0.02 microg/mL). The purification of this bioactive fraction FE was carried out by RP-HPLC affording six sub-fractions 1-6, and only sub-fraction 5 kept the anti-proliferative activity. Its major constituent was identified as quercetin (IC(50)=0.49+/-0.12 microg/mL) by means of HPLC/UV/MS and co-elution with the authentic standard. Quercitrin was also identified in the fraction FE but was inactive. A structure-activity relationship with flavonols determined that methylation reduced the anti-proliferative activity whereas glycosylation abolished it. The present study shows that the anti-proliferative properties of Euphorbia stenoclada are mediated through the presence of quercetin that may explain the traditional use of this plant as a remedy against asthma.

Anti-Asthmatic Agents↗

PubMed2006

Cellular mechanisms of the protective effect of polyphenols on the neurovascular unit in strokes.

Increasing evidence has suggested that our view of stroke should be integrative, and thus a concept of dynamic interaction between cells belonging to the neurovascular unit, such as endothelial cells, astrocytes and neurons, is emerging. The functionality of this unit is altered by the complex series of interconnected pathophysiological processes that damage the brain tissue during this kind of attack. The new strategies target both the preservation of endothelium integrity and the deleterious effects induced by ionic imbalance, excitotoxicity, and the generation of reactive oxygen species within the neurovascular unit. Polyphenols exert numerous biological effects that might participate in the protection of the neurovascular unit, including anti-aggregatory platelet activity, antioxidant and free radical scavenging properties. Moreover, polyphenols are powerful vasodilators through the generation of NO, and can act on the expression of genes protective of the cardiovascular system. Also, polyphenols contribute to the preservation of the integrity of cells belonging to the neurovascular unit, mainly the endothelium, by acting on the signaling cascades implicated in endothelial apoptosis. All these effects of polyphenols might interfere with atherosclerotic plaque development and stability, vascular thrombosis and occlusion and therefore might explain their vascular- and neuroprotective properties. In this review, we focus on the beneficial effects of polyphenols on the complex pathophysiological events of stroke and helpful indications for the design of an effective and well-tolerated therapy will be discussed.

Animals↗

PubMed2006

Origin and biological significance of shed-membrane microparticles.

Microparticles (MPs) are small vesicles released from the membrane surface during eukaryotic cell activation or apoptosis. They originate from various cell types, displaying the typical surface cell proteins and cytoplasmic components of their cell origin. Their procoagulant properties are linked to phosphatidylserine exposed at their surface. Numerous reports have shown that MPs are able to mediate long-range signaling, acting on different targets from those of their own cellular origin. MPs-mediated binding to other cells occurs by integration into the membrane, by adhesion to the cell surface or by ligand-receptor interaction. Elevated levels of circulating MPs have been detected in cardiovascular and immune-mediated diseases. Despite extensive studies of the procoagulant and pro-inflammatory properties of MPs, little is known about their effect on vascular function. MPs accumulate in atherosclerotic plaques and injured vascular wall. Circulating MPs from patients with myocardial infarction induce endothelial dysfunction by impairing the endothelial nitric oxide (NO) pathway, without causing changes in endothelial NO-synthase (eNOS) expression. However, MPs from T-cells may induce endothelial dysfunction, altering gene expression of eNOS and caveolin-1. Moreover, MPs may promote the expression of pro-inflammatory proteins implicated in vascular contractility alterations. This review describes the origin of MPs and their biological role in physiological conditions and in various pathological states, with special reference to the possible linkage between their pro-inflammatory and procoagulant properties and vascular dysfunction.

Animals↗

PubMed2006

Beneficial effects of Provinols: cardiovascular system and kidney.

Red wine polyphenols have been reported to exert beneficial effects in preventing cardiovascular diseases but their molecular mechanisms of hemodynamic effects on functional cardiovascular and renal changes were studied much less. The review is focused on in vitro as well as in vivo effects of red wine extract containing polyphenolic compounds (Provinols) on cardiovascular systems and kidney in relation to the molecular and biochemical mechanisms of these compounds. This review provides the evidence that Provinols is able to produce ex vivo endothelium-dependent relaxation as a result of enhanced NO synthesis. Administration of Provinols partially prevents the development of hypertension during NO deficiency and accelerates the decrease of blood pressure in already established hypertension. The effects of Provinols include prevention and/or attenuation of myocardial fibrosis, reduction of aortic wall thickening and improvement of vascular functions. These functional and structural alterations are associated with significant augmentation of NO production, seen as the increase of NO synthase activity and eNOS protein expression. Moreover, it has been documented that Provinols decreased the oxidative stress within the cardiovascular system and kidney.

Animals↗

PubMed2006

The effect of different antioxidants on nitric oxide production in hypertensive rats.

The imbalance between nitric oxide (NO) and reactive oxygen species (ROS) production appears to be a common feature of experimental and human hypertension. Previously, different antioxidants and/or scavengers of oxygen free radicals were shown to activate nitric oxide synthase (NO synthase, NOS) and to increase the expression of both endothelial and neuronal NO synthase isoforms leading to blood pressure reduction. On the other hand, various antihypertensive drugs have been documented to possess antioxidant properties, which may contribute to their beneficial effect on blood pressure. This review is focused on the effects of antioxidant treatment in different models of experimental hypertension with a special attention to the prevention of oxidative damage and the augmentation of NO synthase activity and expression of NOS isoforms.

Animals↗

PubMed2006

The time-dependent effect of Provinols on brain NO synthase activity in L-NAME-induced hypertension.

Red wine polyphenols have been reported to possess beneficial properties for preventing cardiovascular diseases but their neuroprotective effects during chronic L-NAME treatment have not been elucidated. The aim of this study was to analyze a time course of Provinols effects on brain NO synthase activity and oxidative damage in L-NAME-induced hypertension. Male Wistar rats, 12 weeks old, were divided into six groups: control groups, groups treated with N(G)-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg/day) for 4 or 7 weeks and groups receiving Provinols (40 mg/kg/day) plus L-NAME for 4 or 7 weeks. At the end of the treatment, marker of membrane oxidative damage - conjugated dienes (CD) in the brain and NO synthase activity in the cerebral cortex, cerebellum and brainstem were determined. L-NAME treatment for 4 or 7 weeks led to the increase in blood pressure, elevation of CD concentration and decrease of NO synthase activity in the brain parts investigated. Provinols partially prevented blood pressure rise and elevation of CD concentration. Comparing to the L-NAME treated group, Provinols increased NO synthase activity after 4 weeks of treatment. However, the prolonged Provinols treatment for 7 weeks had no effect on NO synthase activity decreased by L-NAME treatment. In conclusion, Provinols partially prevents L-NAME induced hypertension via the different mechanisms depending on the duration of treatment. Prevention of oxidative damage in the brain with modulating effect on NO synthase activity is suggested.

Animals↗

PubMed2006

Vascular effects of red wine polyphenols in chronic stress-exposed Wistar-Kyoto rats.

Present study investigated the effect of red wine polyphenolic compounds (Provinols) on blood pressure (BP), nitric oxide synthase (NOS) activity and vascular function in Wistar-Kyoto (WKY) rats exposed to chronic social stress produced by crowding. Adult male rats were divided into four groups: control (480 cm(2)/rat), Provinols-treated (20 mg/kg/day, 480 cm(2)/rat), crowded (200 cm(2)/rat) and crowded treated with Provinols (20 mg/kg/day, 200 cm(2)/rat) for 8 weeks. No differences in BP were observed among the groups at the end of experiment, however, reduced BP was observed in Provinols-treated rats after 3 weeks of treatment. NOS activity in the aorta was significantly elevated in crowded rats, while Provinols alone had no effect on nitric oxide (NO) production. Acetylcholine-induced relaxation of the femoral artery was significantly improved in stressed and Provinols-treated rats vs. control, without significant changes in their noradrenaline-induced vasoconstriction. Interestingly, Provinols blunted the elevation of NO production and vasorelaxation during crowding. Increased endothelium-dependent vasorelaxation and NO synthesis in crowded rats may represent the adaptation mechanisms, resulting in unaltered blood pressure in stress-exposed normotensive rats. This study further demonstrated that elevated release of NO during chronic stress may be prevented by Provinols. Thus, Provinols might maintain equilibrium between endothelium-derived vasoconstrictor and vasodilator factors in stress.

Animals↗

PubMed2005

Red wine polyphenols prevent endothelial damage induced by CCl4 administration.

It became evident in the present study that carbon tetrachloride (CCl(4)), in addition to its known liver and renal toxicity, causes serious damage to endothelial cells. The preventive effect of red wine on cardiovascular diseases has been documented in a number of human population studies as well as in animal experimental models. In this study, the endothelium protective effect of polyphenolic compounds isolated from red wine was studied in rats administered 0.5 ml of CC(4)/kg body weight intraperitoneally twice a week for 8 weeks. Endothelemia (endothelial cells/10 microl of plasma) was used as the marker of endothelial cell injury in vivo. Chronic CCl(4) treatment for 8 weeks lead to a 3-fold increase of free endothelial cells circulating in the blood when compared to the baseline values (2.5+/-0.3). Parallel oral administration of polyphenols 40 mg/kg/day significantly decreased the endothelemia. Polyphenolic compounds alone did not produce significant changes. Three weeks of spontaneous recovery after the 8-week treatment with CCl(4) did not lead to a marked decrease of endothelemia, but the administration of red wine polyphenols during the 3-week period significantly decreased free endothelial cells in the blood. It can be concluded that long-term administration of CCl(4) may serve as a useful experimental model of endothelial damage. The red wine polyphenolic compounds exert a powerful protective effect on endothelial cells from the injury caused by CCl(4). This effect was documented by decreased endothelemia that corresponded to diminished endothelial cell swelling and detachment evaluated by histology of the vascular intima. The endothelium protective effect may be one of the key factors that contribute to the preventive action of red wine on cardiovascular diseases.

Animals↗

PubMed2005

Mechanism of potentiation by polyphenols of contraction in human vein-engineered media.

The potential of natural dietary polyphenols in the treatment of vascular diseases originating from veins has been suggested in the literature. However, the mechanisms involved to explain the effects of polyphenols are not yet elucidated. Therefore, the aim of this study was to investigate the mechanisms by which polyphenols from red wine (Provinols) modulated contraction in human veins. We took advantage of a human model previously reported as a new tool for pharmacological research, using tissue-engineered techniques allowing the production of vascular media based exclusively on human smooth muscle cells. Thus human tissue-engineered vascular media (TEVM) were produced with cells originating from umbilical cord vein. TEVM were treated with either vehicle or Provinols. Results showed that treatment of TEVM with Provinols significantly potentiated the contractile responses induced by histamine and bradykinin. The potentiating effect of Provinols was not associated with an enhancement of histamine-induced increase in cytosolic calcium; rather, it implied the presence of a Ca(2+)-independent signaling pathway. Pharmacological studies indicated that action of Provinols took place at the level of phospholipase A(2)-Rho-kinase pathway and was associated with an enhancement of myosin light chain kinase activity. These results, obtained using the human TEVM, bring new insights to explain the regulation of venous contraction by polyphenols.

Calcium↗

PubMed2004

Polyphenolic compounds from Cognac induce vasorelaxation in vitro and decrease post-ischaemic cardiac infarction after an oral administration.

The effects of Cognac polyphenolic compounds (CPC) on aorta and isolated heart, the consequences of oral administration on haemodynamic parameters, vascular reactivity and cardiac recovery after ischaemia were investigated. CPC induced an endothelium-dependent vasorelaxation on rat-isolated aorta. This effect was prevented by the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine-methyl ester, but not by the cyclo-oxygenase inhibitor, indomethacin, suggesting the implication of NO pathway. On isolated rat hearts, CPC induced positive inotropic, chronotropic, and lusitropic effect at 10(-4)-10(-2) g/L while at 10(-1) g/L, it had negative lusitropic effect and other parameters returned to baseline values. Oral administration of 40 mg/kg of CPC for 2 weeks did not modify systolic blood pressure and heart rate of rats throughout the treatment. CPC treatment did not affect ex vivo response of isolated thoracic aorta either to the contractile agent noradrenaline or to the endothelial-relaxant agent, acetylcholine. Isolated hearts from treated rats were submitted to 30-min global ischaemia followed by 120 min of reperfusion. Post-ischaemic recovery of functional cardiac parameters was not modified by treatment with CPC. Infarct size measured after the reperfusion in heart from CPC-treated rats was significantly decreased in comparison with hearts from control group. We conclude that in vitro, CPC had NO-dependent vasorelaxant effects and stimulated cardiac function. Oral treatment with CPC appeared to have no impact in vivo on blood pressure, heart rate of the rats or on cardiac contractility ex vivo; however, it could decrease the infarct size after an ischaemia-reperfusion.

Administration, Oral↗

PubMed2004

Wine polyphenols stimulate superoxide anion production to promote calcium signaling and endothelial-dependent vasodilatation.

The present study was aimed to evaluate the mechanisms involved in the vasorelaxant effects of red wine polyphenol compounds (RWPC) in small mesenteric rat arteries. RWPC produce relaxation in small mesenteric arteries. This relaxant effect was abolished by endothelial denudation, NO-synthase blockade with L-NAME and partial depolarization with KCl or L-NAME plus KCl. Incubation with the reactive oxygen species scavenger, superoxide dismutase (SOD) plus catalase, or inhibition of NAD(P)H-dependent oxidoreductases with diphenyleneiodonium also inhibited RWPC induced vascular relaxation. Application of RWPC elicited a transient increase in intracellular calcium concentration ([Ca2+]i) in bovine aortic endothelial cells (BAEC), which was attenuated by a mixture of SOD and catalase. Incubation of BAEC with RWPC increased the SOD inhibitable production of O2-. These results suggest the involvement of O2- in the [Ca2+]i increase evoked by RWPC, leading to the activation of enzymes involved in the release of endothelial relaxant factors and subsequent vasodilatation of resistance arteries.

Animals↗

PubMed2003

Red wine polyphenols induce vasorelaxation by increased nitric oxide bioactivity.

The aim of the present study was to investigate the mechanism of vasorelaxant responses induced by red wine polyphenolic compounds (Provinol). Rings of rat femoral artery with or without functional endothelium were set up in a myograph for isometric recording and precontracted with phenylephrine (10(-5) M). Provinol in cumulative doses (10(-9) to 10(-3) mg/ml) elicited endothelium- and dose-dependent relaxation of the artery with maximal relaxation of 56 per cent at the concentration of 10(-5) mg/ml. The relaxant responses to Provinol correlated well with the increase of NO synthase activity in the vascular tissue after administration of cumulative doses of Provinol (10(-9) to 10(-3) mg/ml). N(G)-nitro-L-arginine methylester (L-NAME, 3x10(-4) M) significantly attenuated the endothelium-dependent relaxation produced by Provinol. Administration of L-arginine (3x10(-5) M) restored the relaxation inhibited by L-NAME. The relaxant responses of Provinol were abolished in the presence of Ca(2+)-entry blocker, verapamil (10(-6) M). Administration of hydrogen peroxide (H(2)O(2)) abolished acetylcholine (10(-5) M)-induced relaxation of the rat femoral artery, while administration of Provinol (10(2) mg/ml) together with H(2)O(2) helped to maintain the acetylcholine-induced relaxation. Provinol only partially affected the concentration-response curve for the NO donor sodium nitroprusside-induced relaxation in rings without endothelium. In conclusion, Provinol elicited endothelium-dependent relaxation of rat femoral artery by the Ca(2+)-induced increase of NO synthase activity and by protecting NO from degradation.

Acetylcholine↗

PubMed2002

[Cellular mechanism of vasculo-protection induced by polyphenols on the endothelium].

Epidemiological studies have suggested that dietary factors, including moderate red wine consumption, might reduce the risk of cardiovascular diseases. The beneficial effect of fruits, vegetables, or red wine may be in part explained by the presence of polyphenols with a multitude of biological activities, including antioxidant and free radical-scavenging properties, anti-aggregatory platelet property and inhibition of vascular smooth muscle cell proliferation. Another therapeutically relevant effect of polyphenols may be their ability to interact with the generation of nitric oxide from vascular endothelium that leads not only to vasodilatation but also to the expression of genes protective of the cardiovascular system. Finally, polyphenols contribute to the preservation of endothelial integrity by acting on the processes implicated in endothelial proliferation, migration and apoptosis. All these effects of polyphenols might interfere with atherosclerotic plaque development and stability, vascular thrombosis and occlusion and therefore might explain their cardio- and vascular protective properties.

Animals↗

PubMed2002

Endothelial COX-1 and -2 differentially affect reactivity of MVB in portal hypertensive rats.

Expression of constitutive and inducible cyclooxygenase (COX-1 and COX-2, respectively) and the role of prostanoids were investigated in the aorta and mesenteric vascular bed (MVB) from the portal vein-ligated rat (PVL) as a model of portal hypertension. Functional experiments were carried out in MVB from PVL and sham-operated rats in the absence or presence of the nonselective COX inhibitor indomethacin or the selective inhibitors of COX-1 (SC-560) or COX-2 (NS-398). Western blots of COX-1 and COX-2 proteins were evaluated in aorta and MVB, and PGI(2) production by enzyme immunoassay of 6-keto-PGF(1alpha) was evaluated in the aorta. In the presence of functional endothelium, decreased contraction to norepinephrine (NE) and increased vasodilatation to ACh were observed in MVB from PVL. Exposure of MVB to indomethacin, SC-560, or NS-398 reversed the hyporeactivity to NE and the increased endothelial vasodilatation to ACh in PVL, with NS-398 being more potent than the other two inhibitors. Upregulation of COX-1 and COX-2 expressions was detected in aorta and MVB from PVL portal hypertensive rats, and increased production of 6-keto-PGF(1alpha) was observed in aorta from portal hypertensive rats. These results suggest that generation of endothelial vasodilator prostanoids, from COX-1 and COX-2 isoforms, accounts for the increased mesenteric blood flow in portal hypertension.

6-Ketoprostaglandin F1 alpha↗

PubMed2001

Ablation of serotonin 5-HT(2B) receptors in mice leads to abnormal cardiac structure and function.

BACKGROUND: Identification of factors regulating myocardial structure and function is important to understand the pathogenesis of heart disease. Because little is known about the molecular mechanism of cardiac functions triggered by serotonin, the link between downstream signaling circuitry of its receptors and the heart physiology is of widespread interest. None of the serotonin receptor (5-HT(1A), 5-HT(1B), or 5-HT(2C)) disruptions in mice have resulted in cardiovascular defects. In this study, we examined 5-HT(2B) receptor-mutant mice to assess the putative role of serotonin in heart structure and function. METHODS AND RESULTS: We have generated G(q)-coupled 5-HT(2B) receptor-null mice by homologous recombination. Surviving 5-HT(2B) receptor-mutant mice exhibit cardiomyopathy with a loss of ventricular mass due to a reduction in number and size of cardiomyocytes. This phenotype is intrinsic to cardiac myocytes. 5-HT(2B) receptor-mutant ventricles exhibit dilation and abnormal organization of contractile elements, including Z-stripe enlargement and N-cadherin downregulation. Echocardiography and ECG both confirm the presence of left ventricular dilatation and decreased systolic function in the adult 5-HT(2B) receptor-mutant mice. CONCLUSIONS: Mutation of 5-HT(2B) receptor leads to a cardiomyopathy without hypertrophy and a disruption of intercalated disks. 5-HT(2B) receptor is required for cytoskeleton assembly to membrane structures by its regulation of N-cadherin expression. These results constitute, for the first time, strong genetic evidence that serotonin, via the 5-HT(2B) receptor, regulates cardiac structure and function.

Adrenergic beta-Agonists↗

PubMed2001

Simvastatin and Ca(2+) signaling in endothelial cells: involvement of rho protein.

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin is able to produce endothelium-dependent relaxation in addition to its lipid-lowering properties. The underlying mechanisms were investigated in bovine aortic endothelial cells (BAEC). Simvastatin induced an increase in cytosolic calcium ([Ca(2+)](i)) in BAEC, by releasing Ca(2+) from intracellular stores sensitive to thapsigargin and ryanodine, and increasing Ca(2+) entry. Simvastatin response was not altered by the phospholipase A(2) inhibitor ONO-RS-082, or the combination of superoxide dismutase plus catalase. However, the response to simvastatin was reduced by the product of HMG-CoA reductase, mevalonate or by the inhibitor of small G proteins of the Rho family, Clostridium botulinum C3 toxin. Thus, increase in [Ca(2+)](i) involving the activation of Rho protein through mevalonate-dependent pathway is essential for the action of simvastatin and might contribute to its beneficial effects against vascular diseases. This study helps elucidate the mechanisms of endothelial factor generation by simvastatin in BAEC.

Aminobenzoates↗

PubMed2001

Potentiation by aminoethylisothiourea of the extra-cellular Ca(2+) component of norepinephrine-induced contraction in rat femoral arteries.

Aminoethylisothiourea (AET) is a potent inhibitor of inducible nitric oxide synthase (NOS). The present study was performed to investigate whether AET and its rearrangement products might modulate vascular contraction independently of its effects as a NOS inhibitor in rat small femoral arteries. AET caused an endothelium-independent increase in contraction induced by norepinephrine (NE). This effect was not affected by either N(omega)-nitro-L-arginine methyl ester, nitro-L-arginine, indomethacin or propanolol, but it was suppressed in Ca(2+)-free medium. AET enhanced extracellular Ca(2+) component of NE-induced contraction, and this effect was prevented by the receptor-mediated Ca(2+) entry blocker, 1-{beta-[3-(p-methoxyphenyl)-propyloxyl]-p-methoxyphenetyl}- 1H-imidaz ole hydrochloride (SK&F 96365), but not by the voltage-dependent Ca(2+) channel blocker, nitrendipine. AET did not alter the response to CaCl(2) in vessels exposed to KCl depolarization. The protein kinase C (PKC) inhibitor, 2-[1-(3-dimethylaminopropyl)indol-3-yl]-3-(indol-3-yl) (GF 109203X), prevented the potentiating effect of AET on the NE response. AET failed to produce an increase in tone in the presence of NE and GTP in permeabilized arteries. Among the AET rearrangement products, mercaptoethylguanidine produced an endothelium-independent increase in the NE response. 2-aminothiazoline had no effect, and guanidinoethyldisulphide produced relaxation. The effect of mercaptoethylguanidine was dependent on extracellular Ca(+) and was prevented by GF 109203X. These results indicate that AET is able to potentiate the contraction to NE in rat femoral resistance arteries independently of its inhibitory effect on either NOS or cyclo-oxygenase. Its effect occurs via an enhancement of SK&F 96365-sensitive Ca(2+) entry. A PKC inhibitor-sensitive mechanism also appears to be involved in the AET effect. Mercaptoethylguanidine potentiates NE response through a mechanism similar to AET.

Animals↗

PubMed2001

[Moderate alcohol consumption and cardiovascular diseases].

While excessive ethanol consumption can result in higher rate of morbidity and mortality resulting from several diseases including cancer and cirrhosis, epidemiological studies suggest that moderate alcohol ingestion reduces the risk of cardiovascular diseases. However, the precise mechanisms by which moderate alcohol consumption protects against coronary heart disease (CHD) is not fully understood. Epidemiological studies suggest that alcohol consumption influences several risk factors for CHD including blood pressure, plasma cholesterol levels, platelet function, and fibrinolytic parameters, preventing both vascular thrombosis and occlusion. Turning to molecular and cellular levels, ethanol has been shown to act on several signal transduction mechanisms involve in the inhibition of smooth muscle cells proliferation and migration and in the activation of the release of vasoactive factors from vascular cells such as nitric oxide (NO). The latter is of importance since NO has been shown to possess antioxidant, antiaggregant properties, to regulate vascular tone and to inhibit both proliferation of smooth muscle cells and adhesion of leukocytes. Altogether, the above mentioned beneficial properties of moderate concentration of ethanol might help to explain the cardio- and vascular protection induced by ethanol. This review compels several bibliographic data concerning the cardiovascular effect of moderate alcohol consumption.

Animals↗