To explore a possible role for adenosine in the pathogenesis of the splanchnic hyperemia of cirrhosis, we administered 8-phenyltheophylline, a specific adenosine receptor antagonist, to rats with biliary cirrhosis caused by bile duct ligation and to control shamoperated rats. Micro-Doppler flow studies showed that a lO-pmol/kg dose of 8-phenyltheophylline completely abolished the superior mesenteric hyperemic response to infusions of exogenous adenosine in both cirrhotic and control rats. Analysis of regional blood flows by radioactive microspheres demonstrated that this dose of 8-phenyltheophylline in cirrhotic rats significantly increased portal tributary vascular resistance by 60% and decreased portal tributary blood flow by 26%. This decrease was entirely the result of a 42% reduction in the intestinal blood flow. 8-phenyltheophylline did not affect cardiac output, arterial pressure or any other extrasplanchnic hernodynamic variables in cirrhotic rats. No detectable effect of 8-phenyltheophylline was seen in sham-operated rats. These results suggest that adenosine may be involved in the genesis of splanchnic hyperemia in cirrhotic rats. (HEPATOLOGY 1992;15:1107-1111.) Cirrhosis is associated with the derangement of circulation, with increased cardiac output and splanchnic blood flow. The splanchnic hyperemia is of more than academic significance because it contributes to the increase in portal pressure and the ensuing complications. The pathophysiological mechanism for the splanchnic hyperemia is unclear, but various humoral factors have been suggested as playing a role (1-3).
Adenosine is an ubiquitous vasodilator that is thought to mediate several physiological phenomena in the splanchnic circulation, including the hepatic arterial buffer response (4, 51, autoregulatory escape (61, postprandial hyperemia (7, 8) and alcohol-induced hy-