Potentiation of hypoxic pulmonary vasoconstriction by ethyl alcohol in dogs.
Pulmonary and systemic hemodynamics and arterial blood gases were measured in anesthetized and mechanically ventilated dogs before and after oral or intravenous administration of ethanol. Increases in mean pulmonary artery pressure and pulmonary vascular resistance occurred. Platelet antiserum-induced thrombocytopenia inhibition of prostaglandin synthesis with meclofenamate, or alpha-adrenergic blockade did not alter the pulmonary pressor response to ethanol. However, the increase in resistance following ethanol was abolished by hyperoxia and potentiated by hypoxia. Thus, it appears that the effect of ethanol is to augment hypoxic pulmonary vasoconstriction, whereas ethanol per se has no independent pulmonary pressor activity.
D000284:Administration, Oral; D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D004285:Dogs; D000431:Ethanol / Q000008:administration & dosage / Q000494:pharmacology*; D000860:Hypoxia / Q000503:physiopathology*; D007275:Injections, Intravenous; D010100:Oxygen / Q000097:blood; D011453:Prostaglandins / Q000378:metabolism; D011652:Pulmonary Circulation / Q000187:drug effects*; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents
D002395:Catecholamines; D011453:Prostaglandins; D014662:Vasoconstrictor Agents; D000431:Ethanol; D010100:Oxygen