RESUMO
An intravenous infusion of norepinephrine, 2 microgram/kg/min, for 5 hr in anesthetized, mechanically ventilated dogs produced a statistically significant increase in the pulmonary shunt, the cardiac output, and the mean pulmonary artery pressure, but no significant change in the pulmonary wedge pressure and the pulmonary vascular resistance except at 5 min. These hemodynamic changes are qualitatively similar to those produced by the same dose of epinephrine infused for the same time period. However, there were differences in the magnitude of the hemodynamic changes between norepinephrine and epinephrine, as might on the basis of their different pulmonary pharmacologic effects, but the changes were not statistically significant at all times, and more studies are necessary to determine if the differences are real. These studies add support to the thesis that adrenergic stimulation plays an important role in the pathogenesis of the pulmonary insufficiency associated with shock.
Assuntos
Epinefrina/farmacologia , Hemodinâmica/efeitos dos fármacos , Norepinefrina/farmacologia , Circulação Pulmonar/efeitos dos fármacos , Animais , Pressão Sanguínea/efeitos dos fármacos , Débito Cardíaco/efeitos dos fármacos , Cães , Artéria Pulmonar/efeitos dos fármacos , Choque/fisiopatologia , Resistência Vascular/efeitos dos fármacosRESUMO
Twelve healthy, anesthetized, mechanically ventilated dogs received an infusion of isoproterenol hydrochloride, 0.1 microgram per kilogram for two hours. There was a rapid and statistically significant increase in the pulmonary shunt, cardiac output and mean pulmonary artery pressure; a significant decrease in the pulmonary vascular resistance, and no significant change in the pulmonary artery wedge pressure. These findings support those of previous studies which demonstrated the beta adrenergic stimulation is important in the pathogenesis of pulmonary insufficiency. The shunt results from ventilation-perfusion inequalities produced by the increased pulmonary blood flow and pulmonary vasodilatation. Because of the production of pulmonary insufficiency, isoproterenol or other beta adrenergic agonists should be used with caution in the critically ill, who often have or may develop the respiratory distress syndrome.
