Effects of vasodilators on canine cardiopulmonary function when a decrease in cardiac output complicates an increase in right ventricular afterload.

Abstract

In canine oleic acid pulmonary edema, we investigated acute cardiopulmonary effects of nitroprusside (NP) before (NP1), and after (NP2) pulmonary vascular resistance (PVR) was increased via glass bead embolization. In the setting of increased PVR and reduced cardiac output (CO), acute cardiopulmonary effects of NP and hydralazine were compared. Oleic acid increased (p less than 0.05) pulmonary shunt (Qs/Qt) from 15 to 24%, but did not alter PVR. Cardiac output decreased (p less than 0.01) 31% with oleic acid from 4.2 to 2.9 1 X min-1 and systemic vascular resistance (SVR) increased (p less than 0.01). When PVR was normal, NP reduced (p less than 0.05) blood pressure (BP) from 148 to 123 mmHg, decreased SVR 31%, and increased (p less than 0.05) CO and Qs/Qt. Glass bead embolization increased (p less than 0.001) PVR from 2.2 to 20 mgHg X 1-1 X min and reduced (p less than 0.01) CO 23%, from 2.6 to 2 L/min. The Qs/Qt did not increase with embolization. In contrast to effects of NP1, when RV afterload was increased, CO fell (p less than 0.05) with NP2 from 2 to 1.6 1 X min-1. Alternatively, hydralazine improved cardiopulmonary function. In the setting of increased RV afterload, SVR and PVR decreased (p less than 0.01) 48 and 29%, respectively, with hydralazine. Corresponding to the decrease in resistance, CO increased (p less than 0.001) 84% with hydralazine, from 1.9 to 3.5 1 X min-1. Also, BP and Qs/Qt remained constant and arterial O2 tension increased (p less than 0.05) with hydralazine, from 113 to 152 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)