EFFECT OF SODIUM-NITROPRUSSIDE ON CARDIOVASCULAR FUNCTION AND PULMONARY SHUNT IN CANINE OLEIC-ACID PULMONARY-EDEMA

The acute effects of nitroprusside were investigated on intrapulmonary shunt (Qs/Qt), cardiac output and left ventricular function in dogs with normal lungs and again after they developed oleic acid pulmonary edema. Before oleic acid, nitroprusside reduced pulmonary capillary wedge pressure (PCWP) and stroke volume and there were no changes in Qs/Qt. Ninety minutes after oleic acid, PCWP, Qs/Qt and systemic vascular resistance increased and stroke volume decreased. Then nitroprusside increased cardiac output by 35% and increased Qs/Qt from 12-18%. After oleic acid, stroke volume increased on nitroprusside from 18-23 ml (P < 0.05) despite reduced preload, as PCWP decreased from 10.4 to 4.4 torr on nitroprusside (P < 0.05). Increased stroke volume may be explained by the reduction in resistive afterload, as nitroprusside reduced systemic vascular resistance from 60 to 34 torr .cntdot. 1-1 .cntdot. min. To the extent that canine oleic acid pulmonary edema represents low pressure edema in patients, nitroprusside is a potential treatment to reduce PCWP, pulmonary microvascular pressure and pulmonary edema while maintaining cardiac output.