Modulation of haemostatic function and prevention of experimental thrombosis by red wine in rats: a role for increased nitric oxide production

Citation
T. Wollny et al., Modulation of haemostatic function and prevention of experimental thrombosis by red wine in rats: a role for increased nitric oxide production, BR J PHARM, 127(3), 1999, pp. 747-755
Citations number
45
Categorie Soggetti
Pharmacology & Toxicology
Journal title
BRITISH JOURNAL OF PHARMACOLOGY
ISSN journal
00071188 → ACNP
Volume
127
Issue
3
Year of publication
1999
Pages
747 - 755
Database
ISI
SICI code
0007-1188(199906)127:3<747:MOHFAP>2.0.ZU;2-J
Abstract
1 The effects of ethyl alcohol and wine (red and white) on haemostatic para meters and experimental thrombosis were studied in rats; NO was evaluated a s a possible mediator of these effects. 2 We found that red wine (12% alcohol) supplementation (8.4 +/- 0.4 ml d(-1 ) in drinking water, for 10 days) induced a marked prolongation of 'templat e' bleeding time (BT) (258 +/- 13 vs 132 +/- 13 s in controls; P<0.001), a decrease in platelet adhesion to fibrillar collagen (11.6 +/- 1.0 vs 32.2 /- 1.3%; P<0.01) and a reduction in thrombus weight (1.45 +/- 0.33 vs 3.27 +/- 0.39 mg; P<0.01). 3 Alcohol-free red wine showed an effect similar to red wine. In contrast, neither ethyl alcohol (12%) nor white wine (12% alcohol) affected these sys tems. 4 All these effects were also observed after red wine i.v. injection (1 ml kg(-1) of 1.4 dilution) 15 min before the experiments. 5 The effects of red wine were prevented by the NO inhibitor, N(omega)nitro -L-arginine-methyl ester (L-NAME). L-arginine, not D-arginine, reversed the effect of L-NAME on red wine infusion. 6 Red wine injection induced a 3 fold increase in total radical-trapping an tioxidant parameter values of rat plasma with respect to controls, while wh ite wine and alcohol did not show any effect. 7 Our study provides evidence that red wine modulates primary haemostasis a nd prevents experimental thrombosis in rats, independently of its alcohol c ontent, by a NO-mediated mechanism.