FIGURE 8.6. Responses in one cat to intravenous isoproterenol infusion showing the change in superior mesenteric arterial conductance (SMAC) and hepatic arterial conductance (HAC) expressed as a percentage of the maximal vasodilator responses seen with intra-arterial isoproterenol infusions for each artery.

FIGURE 8.6

Responses in one cat to intravenous isoproterenol infusion showing the change in superior mesenteric arterial conductance (SMAC) and hepatic arterial conductance (HAC) expressed as a percentage of the maximal vasodilator responses seen with intra-arterial isoproterenol infusions for each artery. The response of the HA is shown first with SMA flow allowed to rise and thus represents the net effect of the constriction induced by the hepatic arterial buffer response (HABR) and the direct dilator effect of the drug (HAC + HABR). When SMA flow was returned, by clamp, to preinfusion control levels, thus eliminating any HABR constrictor stimulus, the HA dilated to similar levels as the SMA (HAC). The HA response was suppressed by more than 50% through action of the HABR and, at some doses, actually led to a net vasoconstriction. When drugs are administered intravenously, the effect on the hepatic artery is conflicted as the direct drug effect will be countered by the effect of the drug on portal blood flow and the HABR. Reproduced with permission from Lautt WW, d’Almeida MS, McQuaker J, D’Aleo L. Impact of the hepatic arterial buffer response on splanchnic vascular responses to intravenous adenosine, isoproterenol, and glucagon. Can J Physiol Pharmacol 66(6): pp. 807–813, 1988. © 2008 NRC Canada or its licensors. (This figure from publication Can J Physiol Pharmacol is reproduced with permission from publisher NRC Canada).

From: Chapter 8, In Vivo Pharmacodynamic Approaches

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Hepatic Circulation: Physiology and Pathophysiology.
Lautt WW.
San Rafael (CA): Morgan & Claypool Life Sciences; 2009.
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