Protective effect of heat shock pretreatment with heat shock protein induction before hepatic warm ischemic injury caused by Pringle's maneuver

Surgery. 1995 Sep;118(3):510-6. doi: 10.1016/s0039-6060(05)80367-8.

Abstract

Background: Induction of heat shock proteins is thought to have a > cytoprotective effect against environmental stress and to result in a better ischemic tolerance. The protective ability of heat exposure and heat shock protein 72 (HSP 72) induction before warm ischemia caused by Pringle's maneuver was evaluated in rats.

Methods: Heat exposed rats (HS) were compared with control animals (C). The gene expression (messenger RNA) of HSP 72 and HSP 72 were detected by Northern and Western blot analyses. During 40 minutes of in situ reperfusion, liver energy metabolism and levels of standard liver enzymes were evaluated. The survival rate was determined after postoperative day 7.

Results: After heat exposure and recovery, messenger RNA of HSP 72 and HSP 72 can be detected strongly in HS group but not in C group. During reperfusion HS group exhibited a significantly (p < 0.01) improved energy metabolism, and the release of liver enzymes was significantly (p < 0.001) reduced compared with C group. Seven-day survival rate was 100% in HS group but at 50% was significantly impaired (p < 0.05) in C group.

Conclusions: Heat exposure associated with HSP induction has a significant protective effect against warm ischemic liver injury, which results in a relevant improvement of survival rate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Heat-Shock Proteins / biosynthesis*
  • Hot Temperature*
  • Ischemia / complications*
  • L-Lactate Dehydrogenase / blood
  • Liver / blood supply*
  • Liver / surgery*
  • Male
  • Postoperative Complications / prevention & control*
  • Rats
  • Rats, Wistar

Substances

  • Heat-Shock Proteins
  • Adenosine Triphosphate
  • L-Lactate Dehydrogenase