[The effect of nicotine on the hemodynamics and oxygen consumption of the heart following acute and chronic sympathetic blockade and atropine].
In 22 artificially ventilated morphine-urethane-chloralose anesthetized dogs (body weight 17--25 kg) the effects of nicotine (0.01 mg/kg x min i.v. over a 5-min period) on the time course of changes in hemodynamics, contractility and oxygen consumption of the heart were examined before and after acute and chronic pretreatment with sympatholytic agents and with atropine. The purpose of this study was to evaluate quantitatively the different components of the hemodynamic overall effect of nicotine in the intact animal. Our results demonstrate that the increase in myocardial oxygen consumption is mediated predominantly by indirect effects of nicotine (adrenergic and vagal effects). In doses comparable to the nicotine consumption of cigarette smokers, this increase is about 20%. Comparatively, the increase in myocardial oxygen consumption mediated by direct nicotine effects is quantitatively small.
D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects; D004285:Dogs; D004347:Drug Interactions; D006321:Heart / Q000187:drug effects*; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D009538:Nicotine / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects; D013565:Sympatholytics / Q000494:pharmacology*
D013565:Sympatholytics; D001262:Atenolol; D009538:Nicotine; D001285:Atropine
Untersuchungen zur Wirkung von Nikotin auf Hämodynamik und Sauerstoffverbrauch des Herzens nach akuter und chronischer Sympathikolyse und nach Atropin.