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(Circulation. 1997;96:4415-4423.)
© 1997 American Heart Association, Inc.

Articles

Regulation of Hepatic Vascular Volume

Contributions From Active and Passive Mechanisms During Catecholamine and Sodium Nitroprusside Infusion

Harald Kjekshus, MD; Cecilie Risoe, MD, PhD; Tim Scholz, MD; ; Otto A. Smiseth, MD, PhD

From the Institute for Surgical Research, the National Hospital, University of Oslo (Norway).

Correspondence to Harald Kjekshus, Institute for Surgical Research, The National Hospital, N-0027 Oslo, Norway.

Background 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.

Methods and Results 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 µg · kg body weight (bwt)^-1 · min^-1 intraportally) significantly reduced hepatic blood volume by 3.3±1 and 4.3±1 mL · kg bwt^-1, respectively. Nitroprusside (8 and 18 µg · kg bwt^-1 · min^-1 intraportally) increased hepatic blood volume by 1.1±0.2 and 1.9±0.3 mL · 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. Compliance was unchanged. Phenylephrine but not isoprenaline yielded similar results as norepinephrine.

Conclusions The pig model used in this study, accurately quantified hepatic capacitance. -Adrenergic stimulation decreased and nitroprusside increased capacitance by changing unstressed blood volume. These changes in capacitance correspond to expulsion of 300 mL and pooling of 130 mL of blood, respectively, in a 70-kg individual, reflecting that the liver is not only a passive blood reservoir but can respond actively and vigorously to pharmacological interventions.

Key Words: sodium nitroprusside • catecholamines • blood volume • liver circulation • veins

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