As vasopressin began to be used widely to control gastrointestinal hemorrhage, there was concern over the effect of vasopressin on the hepatic circulation. Although an initial vasoconstrictor effect of the drug has been described on the hepatic artery, a secondary increase in blood flow ensues. This increase has been attributed to the accompanying decrease in portal blood flow produced by vasopressin. The present study was done to investigate the mechanism of the response of hepatic artery to vasopressin in dogs. Anesthetized dogs were studied with flow probes placed on hepatic, superior mesenteric, femoral, and renal arteries, and the animals were prepared so that portal blood was diverted into jugular vein, with portal inflow to liver delivered at varying rates with blood pumped from a femoral artery. Vasopressin (0.5-1.0 U/kg) was administered intravenously. Results in dog indicate the biphasic response of hepatic artery blood flow to vasopressin is not dependent on changes in portal blood flow. Rather, it appears to be a characteristic response of this vessel. The biphasic response was not observed in other vascular beds studied and was not modified by atropine. beta-Adrenergic blockade enhanced the vasoconstrictor portion of the response, but this did not significantly alter the secondary blood flow increase.
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