Norepinephrine on venous compliance and unstressed volume in cat liver
- 1 April 1985
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 248 (4) , H468-H476
- https://doi.org/10.1152/ajpheart.1985.248.4.h468
Abstract
Hemodynamic relationships between flows, pressures, and blood volume were examined in the denervated liver of cats anesthetized with pentobarbital. Portal and hepatic lobar venous pressures, portal and total hepatic flows and hepatic blood volume were recorded when portal flow was varied from 0 to 240 ml/min 100 g/liver and when hepatic outflow pressure was varied from 0-9.5 mmHg, before, during, and after i.v. infusion of norepinephrine (2 .mu.g/min .cntdot. kg/body wt). Portal pressure was 1-2 mmHg higher than lobar venous pressure and 8-9 mmHg higher than inferior vena caval pressure, showing that the major site of resistance in the portal circuit was in the large hepatic veins. Intrahepatic pressure was linearly related to total hepatic flow; and norepinephrine increased the intercept but not the slope of this relationship. Hepatic blood volume was linearly related to intrahepatic pressure with a calculated compliance of 2.5-3.0 ml/mmHg .cntdot. 100 g/liver and a calculated unstressed volume at zero pressure of 10-15 ml/100 g liver. Norepinephrine did not significantly change vascular compliance but caused a marked reduction of 15-20 ml/100 g liver in calculated unstressed volume. Norepinephrine reduced hepatic blood volume by 15-20 ml/100 g liver at any given intrahepatic pressure. Apparently, venoconstriction in the hepatic bed occurs by a decrease in unstressed volume with little change in compliance. Unstressed volume represents a true blood volume reserve, independent of passive influences, which can be mobilized by the CNS.This publication has 12 references indexed in Scilit:
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