Escape of the Liver Vasculature From Adrenergic Vasoconstriction

The phenomenon of autoregulatory escape has been described in several vascular beds (1–7), but only in cat small intestine has it been extensively studied (1, 5–7). Electrical stimulation of sympathetic nerves or infusion of norepinephrine results in an initial decrease in intestinal blood flow, which tends to be reversed if stimulation or infusion is continued over a period of several minutes. Accumulation of vasodilator metabolites (1), and activation of beta receptor sites (6), as well as other explanations have been presented. Although many studies have been done on autonomic responses of liver vessels, in only one has autoregulatory escape been reported. Greenway, Lawson and Mellander (2) have found in the cat liver pronounced escape of the hepatic arterial bed during electrical stimulation of the hepatic nerve and also report some observations on escape during hepatic arterial infusion of norepinephrine. The study presented here is a much more extensive investigation of this problem using an in situ, autoperfused canine liver preparation.Methods.Dogs weighing 20 kg or over were anesthetized with sodium pentobarbital at an initial intravenous dose of 30 mg/kg. An incision was made below the right costal margin exposing the liver and major vessels of the upper abdomen. A region of the hilum of the liver was carefully dissected and an area of common hepatic artery and portal vein cleared. The hepatic nerve was ligated and cut. The gastroduodenal artery was doubly tied and sectioned between the most distal of the proper hepatic arteries and the origin of the right gastric artery. An intravenous dose of heparin (500 U/kg) was given at this time. The common hepatic artery was ligated, cannulated (PE 320 tubing) toward the liver, and then perfused from a femoral artery by way of a short length of 1/8 in. i.d. Silastic rubber tubing.