Pulmonary Vascular Response to Sodium Nitroprusside in Anesthetized Dogs

Abstract

The influence of sodium nitroprusside (SNP) infusion on pulmonary hemodynamics and total calculated pulmonary vascular resistance was examined in chloralose anesthetized, spontaneously breathing, normoxic and hypoxic closedchest dogs previously instrumented to record pulmonary arterial pressure and flow. Dose-response curves for pulmonary and systemic vascular resistance were determined in the control state and at each of 7 doses of SNP administered as a continuous IV infusion. Dose-response data were determined before and after sympathetic blockade with propranolol and phentolamine. Prior to sympathetic blockade, systemic arterial pressure and calculated systemic vascular resistance decreased progressively with the dose of SNP. Following autonomic blockade, the fall in systemic arterial pressure was enhanced while systemic vascular resistance declined further. In contrast to the systemic circulation, pulmonary vascular resistance tended to increase progressively with the dose of SNP, rising from 4.21 (± 0.5 SEM) to a maximum of 5.02 (± 0.48 SEM) mm Hg/ml/min .10−2. Following sympathetic blockade, pulmonary vascular resistance increased further during SNP infusion, rising from 4.79 (± 0.64 SEM) to 6.40 (± 1.1 SEM) mm Hg/ml/min .10−2. Changes in pulmonary vascular resistance were not significantly affected by sympathetic blockade. On the other hand, infusion of SNP during conditions of enhanced pulmonary vasoconstriction induced by breathing 5% O2 resulted in a significant fall in pulmonary arterial mean pressure and a significant decrease in calculated vascular resistance. It is concluded that, in the normal lung, SNP may alter pulmonary vascular resistance via extrinsic mechanisms arising from the associated fall in mean left atrial pressure and venous return, whereas in the hypoxic vasoconstricted lung the predominant effect is a reduction in mean pulmonary arterial pressure and a decrease in total pulmonary vascular resistance due to direct pulmonary vasodilatation.