VENTILATION-PERFUSION AND GAS-EXCHANGE EFFECTS OF SODIUM-NITROPRUSSIDE IN DOGS WITH NORMAL AND EDEMATOUS LUNGS

This study was designed to investigate the mechanism by which sodium nitroprusside (SNP) decreases oxygenation by determining its effects on venous admixture [Q(VA)/Qt] and ventilation-perfusion distribution [V(A)/Q] in animals with normal and abnormal lungs. SNP was infused into seven dogs anesthetized with pentobarbital. Mean blood pressure was decreased by 40 per cent during normal lung function and again after the production of diffuse pulmonary edema by intravenous administration of oleic acid. Measurements of blood-gas values, Q(VA)/Q(t) and V(A)/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 per cent oxygen in each pulmonary condition. SNP caused no change in cardiac output [Q(t)] 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 Pa(o2) from 71 ± 7 torr (mean ± 1 SD) to 61 ± 11 torr (P < .01), and increased Q(VA)/Q(t) (oxygen method) from 20 ± 8 to 38 ± 18 percent (P < .01). The increase in Q(VA)/Q(t) correlated well with a 28 percent decrease in pulmonary vascular resistance (PVR) (r = -.863). During pulmonary edema with air and ventilation SNP increased V(A)/Q maldistribution, but during ventilation with oxygen, SNP caused no significant change in Q(s)/Q(t), PVR, or V(A)/Q. The increase in Q(VA)/Q(t) and increase in perfusion to low V(A)/Q regions seen only in animals with pulmonary edema during ventilation with air are compatible with the hypothesis that nitroprusside impairs pulmonary gas exchange by inhibiting hypoxic vasoconstriction, thus increasing V(A)/Q maldistribution.