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 (Ql), lymph (C1), and plasma (Cp) protein concentrations and segmental blood flow (Qb) were measured. Permeability changes were characterized by the minimal Cl Cp 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 Cl Cp 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.
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