Regulation of Hepatic Vascular Capacitance

Abstract

The mammalian liver is part of the splanchnic bed that provides a highly significant blood reservoir for compensation for loss of blood from the thorax and consequently a decreased cardiac output. Stresses requiring blood volume compensation include: blood or water loss, quiet standing, return from a prolonged bout of zero gravity, thermal stress, or exercise. Hepatic blood volume is changed passively by changes in hepatic arterial or gastrointestinal blood flow or by changes in vena caval pressure. Liver blood volume is also changed actively via reflexes, hormones, or drugs that activate the hepatic venous smooth muscle. Hepatic vascular compliance is about ten times that of the body as a whole, and is changed by active mechanisms. The hepatic unstressed blood volume is markedly changed by hormones. Baroreceptor control of hepatic volume is important in dogs, but not in cats and possibly not in humans. The hepatic venular pressure of rats, rabbits, and puppies is about 40% of the pressure gradient between the portal vein and vena cava. Major areas of uncertainty include: (a) the magnitude of sinusoidal pressure and how it is controlled, (b) the mechanisms controlling hepatic venous resistance, and (c) the mechanisms influencing hepatic vascular capacitance.