Hepatic Circulation during Sodium Nitroprusside Infusion in the Dog

Open Access
Publisher Website
Google Scholar
Abstract
Changes in the hepatic circulation and O2 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 flowmeters. Aortic, portal and hepatic vein pressures were recorded, and pH, PCO2 [partial pressure of CO2], 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 .mu.g/kg per min, decreased mean arterial blood pressure as much as 15% with no significant change in hepatic circulation. Doses of 10-20 .mu.g/kg per min decreased arterial blood pressure 40%, portal pressure 44%, and portal blood flow 25%. Hepatic arterial blood flow increased 13%. There was no significant change in O2 content of arterial, portal or hepatic vein blood, in O2 consumption of the liver, or in the ratio of lactate to pyruvate produced by the liver. Concentrations of more than 25 .mu.g/kg per min decreased arterial blood pressure more than 50% from control level, decreased portal and hepatic arterial blood flows as much as 80 and 40%, respectively, and decreased O2 content of portal and hepatic vein blood as much as 5 ml O2/100 ml blood. In conditions of steady portal blood flow infusion of SNP led to a decrease in portal pressure by 18% and a decrease in hepatic arterial blood flow. SNP in concentrations that decrease systemic blood pressure as much as 40% 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.