MECHANISM OF THE INCREASED VASCULAR CAPACITY PRODUCED BY MILD PERFUSION HYPOTHERMIA IN THE DOG

The mechanism of the increased vascular capacity produced by perfusion hypothermia was investigated in 20 anesthetized dogs. A right heart bypass preparation separated cardiac output (CO) into splanchnic (Qs) and nonsplanchnic (termed peripheral, Qp) flows. Each channel drained by gravity into an external reservoir. Blood was then returned to the pulmonary artery at a constant flow of 80 ml/kg per min. Venous resistance and compliance of splanchnic (Rvs and Cs) and peripheral (Rvp and Cp) channels were calculated from transient and steady state volume shifts which occurred following rapid drops in venous pressure. Arterial pressure (Pa), hematocrit (H), plasma protein concentration, and changes in reservoir volume (ΔVres) were also measured. Filtered plasma (VF) volume was determined from changes in hematocrit; ascites (Vas) volume was determined by an indicator dilution technique. Hypothermia to 33°C decreased both Cs and Cp from 0.022 ± 0.002 (mean ± SE) to 0.014 ± 0.001 liter/mm Hg and 0.023 ± 0.002 to 0.017 ± 0.001 liter/mm Hg, respectively. Rvs increased from 7.1 ± 1.0 to 9.0 ± 0.9 mm Hg/liter per min. Portal pressure increased from 7.5 ± 0.4 to 12.9 ± 1.3 mm Hg as H increased from 45.1 ± 1.1 to 49.4 ± 1.5%, and plasma protein concentration increased from 5.1 ± 0.2 to 5.7 ± 0.2 g/100 ml. Rvp, Pa, and the steady state distribution of CO did not change. Vres decreased 0.785 ± 0.063 liter during hypothermia, whereas VF increased 0.321 ± 0.031 liter. Vas increased 0.082 liter during this period. We conclude that a large fraction of the decrease in plasma volume that occurs during mild perfusion hypothermia in the dog can be accounted for by the exudation at the liver of effectively pure plasma. The remaining percentage of filtered volume appears to be lost elsewhere in the circulatory system as an ultrafiltrate. Much of the hypothermia-induced increase in vascular capacity appears to be the result of an increase in the unstressed vascular volume and/or an increase in the volume sequestered in the splanchnic bed by a constriction of the hepatic outflow vessels.