Effects of nitroprusside on venous return and central blood volume in the absence and presence of acute heart failure.

Abstract

The effects of nitroprusside (380-760 .mu.g/min) on the systemic venous return, the central blood volume [CBV] and the equilibrium point between the venous return [VR] and cardiac output [CO] curves were studied in 8 dogs using a right-heart bypass preparation at constant total blood volume. Experiments were performed before and after the production of acute left ventricular failure. During control, nitroprusside infusion shifted the VR curve, with a reduction in its plateau (3.1 to 2.4 l/min; P < 0.005), the CBV fell (-2.4 .+-. 0.4 ml/kg; P < 0.05) and the CO at equilibrium was reduced (3.1 to 2.4 l/min; P < 0.005). Cardiac failure (produced by acute coronary artery ligation) increased the CBV (+6.3 .+-. 0.6 ml/kg; P < 0.01), leading to a decrease in both the systemic blood volume and the plateau of the VR curve (3.2 to 2.6 l/min; P < 0.003). The CO at equilibrium was reduced (3.2 to 1.91 l/min; P < 0.001). In this setting, nitroprusside infusion decreased the CBV (-7.4 ml/kg; P < 0.01), but the VR curve was not altered. The CO curve was markedly shifted upward due to reduced afterload on the failing left ventricle; but in the absence of a downward shift of the VR curve, the CO at equilibrium increased from 1.9-2.6 l/min (P < 0.05). Apparently the differing effects of nitroprusside in acute cardiac failure are due primarily to an increased shift of blood from the central circulation in the failure state compared with the normal circulation. This shift counteracts the systemic venodilatation produced by nitroprusside and allows the markedly improved left ventricular function consequent to reduced afterload to be expressed as increased VR and CO.