Mechanism of the increased vascular capacity produced by mild perfusion hypothermia in the dog.

Abstract

The mechanism for increased vascular capacity produced by perfusion hypothermia was studied in 20 anesthetized dogs. A right heart bypass preparation separated cardiac output (CO) into splanchnic (.ovrhdot.Qs) and nonsplanchnic (termed peripheral, .ovrhdot.Qp) flows. Each channel drained by gravity into an external reservoir. Blood was returned to the pulmonary artery at a constant flow of 80 mg/kg.cntdot.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 after rapid drops in venous pressure. Arterial pressure (Pa), hematocrit (H), plasma protein concentration and changes in reservoir volume (.DELTA.Vres) were measured. Filtered plasma (VF) volume was determined from changes in hematocrit; ascites (Vas) volume was determined by an indicator dilution technique. Hypothermia to 33.degree. C decreased both Cs and Cp from 0.022 .+-. 0.002 (mean .+-. SE)-0.014 .+-. 0.001 l/mm Hg and 0.023 .+-. 0.002-0.017 .+-. 0.001 l/mm Hg, respectively. Rvs increased from 7.1 .+-. 1.0-9.0 .+-. 0.9 mm Hg/l.cntdot.min. Portal pressure increased from 7.5 .+-. 0.4-12.9 .+-. 1.3 mm Hg as H increased from 45.1 .+-. 1.1-49.4 .+-. 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 l during hypothermia, whereas VF increased 0.321 .+-. 0.031 l. Vas increased 0.082 l during this period. Apparently a large fraction of the decrease in plasma volume that occurs during mild perfusion hypothermia in the dog can be accounted for by liver exudation 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.