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Venoconstriction of hepatic capacitance vessels during hemorrhage in cats: efferent mechanisms
C V Greenway1, I R Innes, G D Scott
1Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada.
Abstract:
Cats anesthetized with pentobarbital sodium were hemorrhaged (1 ml.min-1.kg body wt-1) until arterial pressure declined to 55 mmHg. Hepatic volume was recorded by plethysmography. In controls, 20 +/- 5 (SD) ml/kg was removed and hepatic volume decreased 3.6 +/- 0.8 ml/kg. Splanchnic nerve section or administration of hexamethonium-atropine reduced hemorrhage volumes (to 10.3 +/- 2.3 and 4.8 +/- 1.8 ml/kg, respectively) and liver volume changes (to 1.5 +/- 0.5 and 0.7 +/- 0.3 ml/kg, respectively). Section of only the hepatic nerves had no effect on hemorrhage volume or the decrease in hepatic volume. Section of the hepatic nerves after removal of the adrenals and kidneys also had no significant effect on hemorrhage volume or the decrease in liver volume. We conclude that the hepatic capacitance response to hemorrhage does not require direct sympathetic venoconstriction of the hepatic capacitance vessels. Changes in inferior vena caval pressure play a significant but small role. The splanchnic nerves (excluding hepatic nerves) play a major role, possibly by splanchnic arteriolar constriction. Whereas the liver comprises only 2.5% of the body weight, it contributed 18% of the hemorrhage volume.
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