Ventilation-Perfusion and Gas Exchange Effects of Sodium Nitroprusside in Dogs with Normal and Edematous Lungs

Abstract

The mechanism by which sodium nitroprusside (SNP) decreases oxygenation was studied by determining its effects on venous admixture (.ovrhdot.QVA/.ovrhdot.Qt) and ventilation-perfusion distribution (.ovrhdot.VA/.ovrhdot.Q) in animals with normal and abnormal lungs. SNP was infused into 7 dogs anesthetized with pentobarbital. Mean blood pressure was decreased by 40% during normal lung function and again after the production of diffuse pulmonary edema by i.v. administration of oleic acid. Measurements of blood-gas values, .ovrhdot.QVA/.ovrhdot.Qt and .ovrhdot.VA/.ovrhdot.Q by the inert-gas-elimination method were taken before, during and after SNP infusion during ventilation with air and then during ventilation with 100% O2 in each pulmonary condition. SNP caused no change in cardiac output (.ovrhdot.Qt) during normal lung function or after the production of pulmonary edema. SNP had no effect on pulmonary gas exchange during normal lung function. During pulmonary edema and ventilation with air SNP decreased PaO2 (O2 partial pressure) from 71 .+-. 7 torr (mean .+-. 1 SD) to 61 .+-. 11 torr (P < .01) and increased .ovrhdot.QVA/.ovrhdot.Qt (O2 method) from 20 .+-. 8 to 38 .+-. 18% (P < .01). The increase in .ovrhdot.QVA/.ovrhdot.Qt correlated with a 28% decrease in pulmonary vascular resistance (PVR) (r, correlation coefficient = 0.863). During pulmonary edema with air and ventilation SNP increased .ovrhdot.VA/.ovrhdot.Q maldistribution but during ventilation with O2 SNP caused no significant change in .ovrhdot.Qs/.ovrhdot.Qt [intrapulmonary shunting], PVR or .ovrhdot.VA/.ovrhdot.Q. The increase in .ovrhdot.QVA/.ovrhdot.Qt and increases in perfusion to low .ovrhdot.VA/.ovrhdot.Q regions are seen only in animals with pulmonary edema during ventilation with air. Apparently SNP impairs pulmonary gas exchange by inhibiting hypoxic vasoconstriction, thus increasing .ovrhdot.VA/.ovrhdot.Q maldistribution.