Mediation by nitric oxide of the stimulatory effects of ethanol on blood flow
Mediation by nitric oxide of the stimulatory effects of ethanol on blood flow
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DOI:
10.1016/s0024-3205(02)01572-2
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发表时间:
2002-05-10
期刊:
影响因子:
6.1
通讯作者:
Lieber, CS
中科院分区:
文献类型:
--
作者:
Baraona, E;Shoichet, L;Lieber, CS
The contribution of nitric oxide (NO) to the hemodynamic effects associated with alcohol oxidation was assessed in rats given either ethanol or water by gastric tube, with and without pre-treatment with either the NO synthase inhibitor N-omega-monomethyl-L-arginine (L-NMMA; 15 mg/Kg i.p.) or the alcohol dehydrogenase inhibitor 4-methylpyrazole (4-MP; 82 mg/Kg i.p.). Alcohol increased plasma NO (measured with chemiluminescence) by 63%. This was prevented by either L-NMMA or 4-MP. Cardiac output and regional blood flows were determined with (57)Cobalt-labeled microspheres. Alcohol markedly enhanced portal blood flow (130 +/- 6 mL/min/Kg vs. 62 +/- 4, in controls; p < 0.01) with no changes in the hepatic, splenic or pancreatic arterial blood flows, indicating that the vasodilatation is mainly mesenteric. In addition, it quadrupled the coronary blood flow, doubled the renal flow and increased cardiac output by 38%, with no significant changes in pulmonary, cerebral or testicular flows. All the stimulatory effects of ethanol on flow, as well as the rise in NO levels, were prevented by L-NMNIA, incriminating NO as the mediator of the hemodynamic effects of ethanol oxidation, acting probably via acetate and adenosine. (C) 2002 Elsevier Science Inc. All lights reserved.