Impact of the hepatic arterial buffer response on splanchnic vascular responses to intravenous adenosine, isoproterenol, and glucagon

Hepatic arteries (HA) and superior mesenteric arteries (SMA) of cats anesthetized with pentobarbital responded to direct intra-arterial infusion of isoproterenol, adenosine, and glucagon with dose-related vasodilation. In response to intravenous infusion, however, the HA failed to dilate significantly, while the SMA dilated thus elevating portal blood flow. The lack of dilation of the HA was due to the HA buffer response to the elevated portal blood flow, that is, elevation of portal flow causes the HA to constrict. When a clamp was used to return SMA flow to control levels during infusion of the drugs, the HA showed significant dilation to all three agents. Thus, HA vascular responses to i.v. drugs can only be assessed if portal flow is known, since the net effect is dependent upon direct action of the drug on the HA as well as the indirect effect of any drug-induced change in portal flow. None of the agents tested altered the magnitude of the HA buffer response obtained during i.v. infusions, but the effects of other agents on the buffer response remain unknown and must be considered in any tests of i.v. administered drugs. Bolus i.v. injections produce results on the HA flow that are uninterpretable.