Venoconstriction of hepatic capacitance vessels during hemorrhage in cats: afferent mechanisms

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. Hemorrhage volume was 21.1 +/- 4.7 (SD) ml/kg, and hepatic volume declined by 4.0 +/- 1.7 ml/kg. These responses were markedly reduced by four procedures that prevented decreases in carotid arterial and central venous pressures and eliminated vagal conduction. When any three of these four procedures were carried out, the remaining stimulus caused a significant increase in the size of the hepatic volume decrease. The results suggest that arterial receptors (baro- and/or chemoreceptors) in the carotid arterial bed or brain and venous baroreceptors in the right atrium and superior and inferior venae cavae are involved in hepatic capacitance responses to hemorrhage. The responses were linearly related to the stimuli, and hepatic blood volume changed by 1.7 +/- 1.1 and 0.030 +/- 0.016 ml/kg for each 1-mmHg change in venous and carotid arterial pressures, respectively. The maximal responses to these afferent stimuli applied individually were not significantly different (-4.2 +/- 1.8 ml/kg) and were not additive, suggesting overlapping redundant systems. The possibility of baroreceptors in superior vena cava has not previously been documented.