Deep Hypothermia Diminishes the Ischemic Induction of Heat-Shock Protein-72 mRNA in Piglet Brain

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Abstract
Background and Purpose Expression of the 72-kD heat-shock protein (HSP72) has served as a useful indicator of ischemic stress after cerebral ischemia. Moderate hypothermia (30°C) has been reported to block the induction of HSP72 after a brief episode of forebrain ischemia. The objective of the present study was to examine the effects of deep hypothermia (15°C) on expression of HSP72 after a prolonged period of cerebral ischemia. Methods Piglets, 19 to 23 days old, were placed on cardiopulmonary bypass, and brain temperature was lowered to 23°C (n=9) or 15°C (n=9) before circulatory arrest for 1 hour. In an additional group of animals (n=5), the temperature was lowered to 29°C before arrest for 45 minutes. All animals were reperfused at 37°C for 2 hours, and the regional expression of HSP72 mRNA was assessed using in situ hybridization. Results After ischemia at 15°C, expression of HSP72 mRNA was limited to a few scattered regions of cerebral cortex; the percentage of cortex exhibiting HSP72 mRNA was 23±7% (mean±SEM). Ischemia at 23°C triggered expression of HSP72 mRNA in a significantly larger portion of the cortex (68±8%, P <.001). Ischemia at 29°C failed to induce substantial expression of HSP72 mRNA in the cerebral cortex. Conclusions These results suggest that, relative to ischemia at 23°C, deep hypothermia (15°C) diminishes ischemic alterations leading to induction of HSP72 mRNA. The lack of cortical expression of HSP72 mRNA following ischemia at 29°C may be secondary to inadequate recovery of energy metabolism.