Hemodynamic actions of nicotine on the canine stomach.

Acute effects of nicotine were determined in the circulation of the stomach in which measurements of gastric blood flow, systemic arterial and portal venous blood pressures, and the arteriovenous oxygen content difference were made. From these measurements gastric vascular resistance and oxygen consumption were calculated. Nicotine was infused for 10-min periods in two doses intraarterially (ia) and intravenously (iv) alone and following adrenergic receptor blockade with either propranolol or phentolamine or both agents. With ia nicotine alone, gastric blood flow and oxygen consumption increased. The effect of nicotine on blood flow was enhanced by prior treatment with phentolamine. The effects of nicotine on both blood flow and oxygen consumption were abolished in the presence of combined phentolamine plus propranolol. With iv nicotine alone, gastric blood flow, oxygen consumption, and arterial pressure increased transiently. Phentolamine enhanced the effect of nicotine on oxygen uptake and prevented the pressor response. Propranolol enhanced the pressor effect of nicotine but abolished the blood flow and oxygen consumption responses. Combined treatment with both adrenergic antagonists abolished nicotine effects on blood flow and oxygen consumption. These findings indicate that nicotine alters gastric hemodynamics and oxygen consumption during acute intravascular infusions of the drug. The vasodilator and metabolic effects of nicotine appear to be mediated via beta-adrenergic receptors. These findings provide little basis for implicating a local ischemic mechanism in the ulcerogenic effects of nicotine on the stomach.