REGULATION OF HEPATIC VASCULAR VOLUME - CONTRIBUTIONS FROM ACTIVE ANDPASSIVE MECHANISMS DURING CATECHOLAMINE AND SODIUM-NITROPRUSSIDE INFUSION

Background It is unclear how the liver contributes to regulation of ca rdiac filling. The aims of this study were to establish an animal mode l to quantify hepatic vascular capacitance and to determine the mechan isms whereby catecholamines and sodium nitroprusside modify hepatic bl ood volume. Methods ann Results In 8 anesthetized pigs we measured hep atic and systemic pressures and flows. Liver vascular volume was measu red by sonomicrometry calibrated against integrated hepatic inflow dur ing outflow occlusion. Pressure-volume (P-V) curves were constructed d uring outflow occlusion. Sonomicrometry accurately reflected hepatic b lood volume (r=.99+/-.001), and hepatic P-V curves were highly reprodu cible. Norepinephrine (0.3 and 0.7 mu g . kg body weight (bwt)(-1) . m in(-1) intraportally) significantly reduced hepatic blood volume by 3. 3+/-1 and 4.3+/-1 mL . kg bwt(-1), respectively. Nitroprusside (8 and 18 mu g . 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. Norep inephrine and nitroprusside parallel shifted the hepatic P-V curves, i ndicating reduced and increased unstressed blood volume, respectively. These curve shifts accounted for more than 90% of the respective bloo d volume changes. Compliance was unchanged. Phenylephrine but not isop renaline yielded similar results as norepinephrine. Conclusions The pi g model used in this study, accurately quantified hepatic capacitance. alpha-Adrenergic stimulation decreased and nitroprusside increased ca pacitance by changing unstressed blood volume. These changes in capaci tance correspond to expulsion of 300 mL and pooling of 130 mL of blood , respectively, in a 70-kg individual, reflecting that the liver is no t only a passive blood reservoir but can respond actively and vigorous ly to pharmacological interventions.