JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Preconditioning somatothermal stimulation on right seventh intercostal nerve territory increases hepatic heat shock protein 70 and protects the liver from ischemia-reperfusion injury in rats.

Hyperthermic preconditioning attenuates the heat-induced cellular response to a subsequent severe heat challenge. However, it is impractical to perform whole-body hyperthermia in humans. This study was designed to test the hypotheses that hepatic heat shock protein 70 (Hsp70) could be induced by local somatothermal stimulation (LSTS) on right seventh intercostal nerve territory and that preconditioning the rats with LSTS protects the liver from subsequent ischemia-reperfusion injury. LSTS was brought about by application of a heating rod above right seventh intercostal nerve territory in male Sprague-Dawley rats. Hepatic gene expression of Hsp70 was assessed by Western blot and reverse transcription polymerase chain reaction (RT-PCR). Finally, serum ALT and AST and the lipid peroxidation product malondialdehyde (MDA) were evaluated in ischemic-reperfused rats preconditioned by application of LSTS on right seventh intercostal nerve territory. The results showed that hepatic gene expression of Hsp70 was upregulated in rats treated with LSTS. When animals were preconditioned with LSTS, followed by subsequent ischemia-reperfusion injury of the liver, there were significant decreases in liver enzymes (ALT/AST) and MDA formation in rats pretreated with one dose of LSTS (LSTS-1 group) as compared with those not treated with LSTS (control group) or treated with three doses of LSTS (LSTS-3 group). We conclude that mild local heat stress (one dose) on right seventh intercostal nerve territory upregulates hepatic gene expression of Hsp70 and protects the liver from subsequent ischemia-reperfusion injury. This might provide an easily applicable method for those patients facing ischemia-reperfusion challenge of the liver, as in liver resection and liver transplantation.

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