Dopamine compensates for deterioration of hepatic hemodynamics and metabolism during occlusion and reperfusion of the hepatic artery.

OBJECTIVE To investigate the effects of temporary hepatic arterial occlusion and dopamine on hepatic hemodynamics and metabolism. DESIGN Experimental animal study in a dog model. The proper hepatic artery was occluded for 60 minutes; then, it was reperfused for 60 minutes. Hepatic hemodynamic and oxygen metabolic values, lactate uptake ratios, and blood glucose levels were determined repeatedly throughout the experiment. Data are given as mean +/- SE. INTERVENTION In another group, dopamine hydrochloride, 10 micrograms/kg per minute, was infused intravenously throughout the experiment, and the same variables were recorded. RESULTS Portal vein blood flow continuously decreased during occlusion, and it decreased even further after declamping of the hepatic artery; this led to a disturbance of oxygen and lactate metabolism in the control group. Dopamine increased the portal vein blood flow from 84.9% +/- 3.9% to 100.9% +/- 3.6% of the preocclusion levels after 60-minute occlusion and from 79.0% +/- 3.6% to 93.6% +/- 5.1% of the preocclusion levels after 60-minute reperfusion (P < .05, respectively). Dopamine also enhanced the hepatic oxygen uptake ratio from 112.8% +/- 12.0% to 150.7% +/- 11.6% of the preocclusion levels after 60-minute reperfusion (P < .05, respectively). These factors contributed to acceleration of the hepatic oxygen consumption and lactate uptake ratio in the group of dogs that were infused with dopamine. CONCLUSIONS Temporary occlusion of the hepatic artery causes deterioration of hepatic hemodynamics and metabolism. Administration of dopamine is an effective way to support hepatic function during occlusion of the hepatic artery.