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Heat-shock preconditioning protects fatty livers in genetically obese Zucker rats from microvascular perfusion failure after ischemia reperfusion
Authors:Kazuhiko?Yamagami,Georg?Enders,Rolf?Josef?Schauer,Rosemarie?Leiderer,J?rg?Hutter,Yuzo?Yamamoto,Yoshio?Yamaoka,Claus?Hammer,Konrad?Messmer  author-information"  >  author-information__contact u-icon-before"  >  mailto:icfsek@icf.med.uni-muenchen.de"   title="  icfsek@icf.med.uni-muenchen.de"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author
Affiliation:Department of Gastroenterological Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Abstract:Reduced tolerance of steatotic livers to ischemic injury is considered to correlate with impaired microcirculation. The aim of this study was to investigate the impact of heat-shock preconditioning (HSPC) on microcirculatory failure after ischemia/reperfusion (I/R) in steatotic livers by means of intra-vital fluorescence microscopy. Obese Zucker rats were used. In the HS group, rats underwent whole-body hyperthermia followed by 60-min partial liver ischemia. In group IR, rats were exposed only to ischemia. Microcirculation parameters (sinusoidal perfusion rate, sinusoidal diameter, leukocyte-endothelial interaction) were significantly better preserved in the HS group than in the IR group. Liver enzymes, oxygenated glutathione/reduced glutathione (GSSG/GSH) ratio, and electron microscopy showed less damage in the HS group. A marked expression of heat shock protein 72 (HSP72) and heme oxygenase (HO-1) was found only in the livers of group HS. HSPC mitigated the I/R injury of steatotic livers by preventing post-ischemic failure of microcirculation. This beneficial effect was found to be associated with the induction of HSP72 and HO-1.
Keywords:Heat-shock preconditioning    Steatotic liver    Liver microcirculation    Intra-vital fluorescence microscopy    Ischemia/reperfusion    Heat shock proteins
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