Yamagami Kazuhiko, Enders Georg, Schauer Rolf Josef, Leiderer Rosemarie, Hutter Jörg, Yamamoto Yuzo, Yamaoka Yoshio, Hammer Claus, Messmer Konrad
Department of Gastroenterological Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Transpl Int. 2003 Aug;16(8):456-63. doi: 10.1007/s00147-002-0519-5. Epub 2003 Apr 16.
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.
脂肪变性肝脏对缺血性损伤的耐受性降低被认为与微循环受损有关。本研究的目的是通过活体荧光显微镜研究热休克预处理（HSPC）对脂肪变性肝脏缺血/再灌注（I/R）后微循环衰竭的影响。使用肥胖 Zucker 大鼠。在 HS 组中，大鼠先进行全身热疗，然后进行 60 分钟的部分肝脏缺血。在 IR 组中，大鼠仅暴露于缺血状态。HS 组的微循环参数（窦状隙灌注率、窦状隙直径、白细胞-内皮细胞相互作用）明显比 IR 组保存得更好。肝酶、氧化型谷胱甘肽/还原型谷胱甘肽（GSSG/GSH）比值以及电子显微镜显示 HS 组的损伤较小。仅在 HS 组的肝脏中发现热休克蛋白 72（HSP72）和血红素加氧酶（HO-1）有明显表达。HSPC 通过防止缺血后微循环衰竭减轻了脂肪变性肝脏的 I/R 损伤。发现这种有益作用与 HSP72 和 HO-1 的诱导有关。
