Hepatic circulation during sodium nitroprusside infusion in the dog.

Abstract

Changes in the hepatic circulation and oxygen supply during sodium nitroprusside (SNP) infusion were studied in 14 dogs anesthetized with pentobarbital, 30 mg/kg. Portal and hepatic arterial blood flows were measured with electromagnetic flow-meters. Aortic, portal and hepatic vein pressures were recorded, and pH, PCo2, O2 content, and lactate and pyruvate concentrations of blood from these vessels were measured. Cardiac output was determined by thermodilution using a Swan-Ganz catheter. In half the dogs a surgical preparation permitted controlled portal blood flow. SNP, 3–5 μg/kg/min, decreased mean arterial blood pressure as much as 15 per cent with no significant change in hepatic circulation, Doses of 10–20 μg/kg/min decreased arterial blood pressure 40 per cent, portal pressure 44 per cent, and portal blood flow 25 per cent. Hepatic arterial blood flow increased 13 per cent. There was no significant change in oxygen content of arterial, portal or hepatic vein blood, in oxygen consumption of the liver, or in the ratio of Iactate to pyruvate produced by the liver. Concentrations of more than 25 μg/kg/min decreased arterial blood pressure more than 50 per cent from control level, decreased portal and hepatic arterial blood flows as much as 80 and 40 per cent, respectively, and decreased oxygen content of portal and hepatic vein blood as much as 5 ml oxygen/100 ml blood. In conditions of steady portal blood flow infusion of SNP led to a decrease in portal pressure by 18 per cent and a decrease in hepatic arterial blood flow. It is concluded that SNP in concentrations that decrease systemic blood pressure as much as 40 per cent of the baseline value does not lead to hepatic hypoxia in normal dogs. SNP decreases portal presinusoidal resistance and does not interfere with the ability of the liver to increase hepatic arterial blood flow in conditions of insufficient portal circulation.