Shimabukuro T, Yamamoto Y, Kume M, Kimoto S, Okamoto R, Morimoto T, Yamaoka Y
Department of Gastroenterological Surgery, Kyoto University Graduate School of Medicine, Japan.
World J Surg. 1998 May;22(5):464-8; discussion 468-9. doi: 10.1007/s002689900417.
The role of heat shock pretreatment in the induction of tolerance for ischemia-reperfusion injury was investigated in rat livers with fibrosis produced by carbon tetrachloride (CCI4) injected subcutaneously. The control group (group C, n = 56) received no pretreatment except anesthesia, and the heat shock group (group HS, n = 56) were exposed to heat shock (42 degrees C) for 15 minutes. After a 48-hour recovery all rats were subjected to 30 minutes of warm ischemia. Western blotting analysis was employed for heat shock protein (HSP) 72 detection. The adenine nucleotide levels in liver tissue and the liver enzyme levels in serum were measured before and after ischemic intervention (seven animals were used at each of six time point measurements in both groups). HSP72 was induced in group HS at greater intensity than in group C. The survival rate on postoperative day 7 in group C (3/14) was significantly poorer than that in group HS (14/14) (p < 0.01). The higher survival rate in group HS was accompanied by more rapid recovery of the adenosine triphosphate level and lower serum levels of liver enzymes after reperfusion (p < 0.01 vs. group C). Heat shock preconditioning induces HSP72 in the rat liver with fibrosis and provides significantly increased tolerance of warm-ischemia reperfusion injury.
在皮下注射四氯化碳（CCI4）诱导产生肝纤维化的大鼠肝脏中，研究了热休克预处理在诱导缺血再灌注损伤耐受性中的作用。对照组（C组，n = 56）除麻醉外未接受任何预处理，热休克组（HS组，n = 56）接受42℃热休克15分钟。48小时恢复后，所有大鼠均经历30分钟的温缺血。采用蛋白质免疫印迹分析检测热休克蛋白（HSP）72。在缺血干预前后测量肝组织中的腺嘌呤核苷酸水平和血清中的肝酶水平（两组在六个时间点测量时，每个时间点均使用七只动物）。HS组中HSP72的诱导强度高于C组。C组术后第7天的存活率（3/14）明显低于HS组（14/14）（p < 0.01）。HS组较高的存活率伴随着再灌注后三磷酸腺苷水平更快的恢复和更低的血清肝酶水平（与C组相比，p < 0.01）。热休克预处理可在纤维化大鼠肝脏中诱导HSP72，并显著提高对温缺血再灌注损伤的耐受性。
