Effect of hydralazine on cardiac output and venous admixture in experimental lung injury.

Abstract

The mechanism by which hydralazine increases venous admixture (QVA/QT) in the setting of lung injury was investigated in a canine model of noncardiogenic pulmonary edema. Permeability pulmonary edema was produced by administration of oleic acid, 0.08 ml/kg given intravenously to 9 mongrel dogs. After stabilization of lung injury, hydralazine was administered intravenously in a loading dose of 1 mg/kg and followed by a constant infusion at 0.05 mg/kg/h. To control for the effect of increased cardiac output (QT) on QVA/QT, a balloon catheter was placed in the inferior vena cava, and stepwise inflation of the balloon was used to impede venous return and maintain QT at predrug levels. Prior to inflation of the balloon catheter, administration of hydralazine produced a 51% decrease in total systemic resistance (TSR) and a 23% decrease in mean arterial pressure (Pa). In contrast, pulmonary vascular resistance (PVR) showed no significant change, and mean pulmonary artery pressure (Ppa) increased 47%. Cardiac output increased from 3.4 +/- 0.3 to 5.5 +/- 0.4 L/min (mean +/- SEM; p less than 0.01) after administration of hydralazine, and QVA/QT increased from 23 +/- 7 to 35 +/- 5% (p less than 0.05). Mean arterial oxygen tension (PaO2) showed no significant change. Inflation of the balloon in the inferior vena cava after hydralazine administration reduced QT to 3.1 +/- 0.4 L/min and QVA/QT to 28 +/- 4%. Neither of these values differed significantly from the prehydralazine levels. Similarly, values for Ppa and PVR after hydralazine administration plus balloon inflation did not differ significantly from predrug levels.(ABSTRACT TRUNCATED AT 250 WORDS)