Regulation of hepatic vascular volume: contributions from active and passive mechanisms during catecholamine and sodium nitroprusside infusion
Abstract
It is unclear how the liver contributes to regulation of cardiac filling. The aims of this study were to establish an animal model to quantify hepatic vascular capacitance and to determine the mechanisms whereby catecholamines and sodium nitroprusside modify hepatic blood volume. In 8 anesthetized pigs we measured hepatic and systemic pressures and flows. Liver vascular volume was measured by sonomicrometry calibrated against integrated hepatic inflow during outflow occlusion. Pressure-volume (P-V) curves were constructed during outflow occlusion. Sonomicrometry accurately reflected hepatic blood volume (r=.99+/-.001), and hepatic P-V curves were highly reproducible. Norepinephrine (0.3 and 0.7 microg x kg body weight (bwt)(-1) min(-1) intraportally) significantly reduced hepatic blood volume by 3.3+/-1 and 4.3+/-1 mL x kg bwt(-1), respectively. Nitroprusside (8 and 18 microg x kg bwt(-1) x min(-1) intraportally) increased hepatic blood volume by 1.1+/-0.2 and 1.9+/-0.3 mL x kg bwt(-1), respectively. Norepinephrine and nitroprusside parallel shifted the hepatic P-V curves, indicating reduced and increased unstressed blood volume, respectively. These curve shifts accounted for more than 90% of the respective blood volume changes...Continue Reading
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