Liver ischemia modifies the concentration of plasmatic catecholamines after reperfusion in the rat

Pulmonary hypertension is one of the most frequent and severe consequences of liver ischemia. The aim of this study is to evaluate the presence of humoral vasoactive mediators, generated during liver ischemia, which could be able to determine the onset of pulmonary hypertension. Thus, we evaluated the plasmatic concentration of catecholamines (adrenaline, noradrenaline, dopamine) during the immediate reperfusion period. Wistar rats were used. Animals (n = 89) were divided into four groups. Group 1 served as control (sham-operated). In group 2 animals underwent 60 min of left hepatic exclusion. In group 3 animals underwent to bilateral adrenectomy. In group 4 animals had both bilateral adrenectomy and liver ischemia. Ischemia in group 2 and 4 was induced by interrupting the vascular supply to the left and median lobes, so avoiding the use of a portal shunt. Blood samples were collected from the suprahepatic inferior caval vein immediately after reperfusion. Strips of the main pulmonary artery were put into an isolated organ bath and tested for the response to noradrenaline, adrenaline and plasma samples. Plasma samples collected after ischemia caused a significantly greater (p < 0.01) contraction of the pulmonary artery compared to controls. Plasma samples collected after adrenectomy caused a weak contraction which was not different from that obtained in the adrenectomy + ischemia group. Plasma concentrations of catecholamines after liver ischemia were significantly increased in the control group (p < 0. 01). In adrenectomized rats only the adrenaline level was greatly reduced. However ischemia did not increase plasma catecholamines as it occurred in sham-operated rats.