Richardson's ground squirrels [body temperature (Tb) 7 degrees C] survive prolonged stable hypothermia for three times as long as do rats (Tb 19 degrees C) (72 vs. 24 h). We have examined the changes in blood gases and acid-base state to assess whether these contribute to this difference in survival time. None of the variables (measured at ambient temperature of 25 degrees C) differed significantly between rats and ground squirrels before hypothermic induction. During cooling, neither hematocrit nor plasma lactate changed significantly, but arterial and venous PO2 and PCO2 increased and arterial and venous pH decreased in both groups. During prolonged hypothermia, hematocrit increased significantly in rats (58.8 +/- 1.7% at 24 h) but not in ground squirrels (39.1 +/- 1.0% at 72 h). Both species maintained stable arterial blood gases but showed decreased venous PO2; arterial and venous pH decreased significantly with time in both species in conjunction with increased plasma lactate. These patterns of decreased venous PO2 and increased plasma lactate suggest that reduced tissue oxygenation occurs during hypothermia. This happens earlier in rats at a Tb of 19 degrees C than in ground squirrels at a Tb of 7 degrees C, possibly as a result of increased hematocrit in hypothermic rats. Remedial measures directed at improving tissue O2 delivery may therefore prolong the hypothermic survival of rats.

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In hypothermia, impairment of metabolic substrate mobilization and utilization may be a factor limiting survival. By use of a newly developed technique, substrate profiles and their regulation by insulin were examined in hypothermic rats (body temperature 19 degrees C) over 24 h. Plasma glucose concentrations increased to approximately 300 mg/dl during cooling and remained high throughout the period of hypothermia. Free fatty acid (FFA) concentration was not altered during cooling or during the first 10 h of hypothermia (approximately 700 mu eq/l) but progressively decreased thereafter, reaching 420 mu eq/l by 20 h. Plasma insulin decreased dramatically during cooling and remained very low (9 +/- 2 microU/ml) during the whole period of hypothermia, reflecting the suppression of insulin secretion by isolated islets at low temperatures. To test he hypothesis that suppression of endogenous insulin secretion may hamper glucose utilization and thus limit survival in hypothermia, exogenous insulin was administered. At doses of 0.1, 0.5, and 1 U/kg intravenously, insulin slowly decreased plasma glucose and FFA. However, at 0.1 and 1 U/kg intraperitoneally, insulin resulted in a dose-dependent decrease in survival time in the hypothermic rat. It is possible that the antilipolytic effect of insulin may have outweighed any beneficial effect of improving glucose utilization in hypothermia.

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