Hypothermia prevents increased capillary permeability following ischemia-reperfusion injury

Abstract

Severely injured trauma victims are frequently hypothermic. It is nuclear, however, whether hypothermia itself is a detrimental or protective physiologic response to injury. One of the major consequences of fluid resuscitation following ischemic injury is edema formation, characterized by ischemia-reperfusion injury models. The purpose of this study was to examine the effect of regional hypothermia on a feline intestinal model of ischemia-reperfusion injury. An autoperfused segment of cat ileum was isolated and arterial, venous, and lymphatic vessels were cannulated. Lymph flow ( Q l), lymph ( C 1), and plasma ( C p) protein concentrations and segmental blood flow ( Q b) were measured. Permeability changes were characterized by the minimal C l C p ratio obtained by elevating venous outflow pressure. Animals were divided into the following groups: Group I: 1 hr of intestinal ischemia (30 mm Hg) with autoreperfusion; Group II: 1 hr of intestinal hypothermia (28°C) with subsequent rewarming; Group III: 1 hr of combined ischemia and hypothermia. Group III animals were either kept hypothermic (IIIA) or rewarmed (IIIB) during autoreperfusion. Minimal C l C p ratios (mean ± SEM) were as follows: Control: 0.15 ± 0.02; Group I∗: 0.32 ± 0.03; Group II: 0.15 ± 0.01; Group IIIA: 0.18 ± 0.02; Group IIIB∗: 0.42 ± 0.02; ( ∗ = P < 0.01 vs control). Reperfusion flow rates were no different between Group IIIA and Group IIIB animals. Ischemia-reperfusion, but not hypothermia alone, caused a marked increase in intestinal capillary permeability. Permeability increased after combined ischemia and hypothermia only if reperfusion was accompanied by rewarming. Hypothermic reperfusion protected against the increased permeability following ischemia.