【摘要】 目的　通过热休克预适应模型 ,观察其是否可以改善心脏保存后心功能的恢复 ,提高心脏的保存质量 ,探讨此模型中心肌保护作用的分子基础。方法　健康成年新西兰白兔 2 0只 ,随机分为两组 ,每组 10只 ,Ⅰ组为对照组 ;Ⅱ组为热休克组 ,将兔体温升高到 42℃ ,保持 15min ,自然环境下恢复 2 4h后处理 ;两组实验方法相同 ,心肌保存前用K H液灌注 35min ,然后用 4℃STS液使心脏停搏并 4℃保存 6h ,保存后用K H复灌 30min。保存前、复灌后于工作心期末测定心率 (HR) ,冠脉流量 (CF)、左室收缩末期压 (LVESP)和左室舒张末期压 (LVEDP) ,心功能恢复率以保存前的百分率表示 ,再灌注期末取心肌组织进行热休克蛋白 72 (HSP72 )的定量和定位检测 ,测定心肌内NO、肌酸激酶同功酶 (CK MB)、乳酸脱氢酶 (LDH)的含量 ,测定超氧化物歧化酶 (SOD )和脂质过氧化物(LPO)的含量 ,测定心肌含水量。结果　热休克组心功能恢复明显好于对照组 ,且与心肌内HSP72含量相关 (r =0 .95 ) ,其心肌内NO含量亦明显高于对照组。结论　热休克预适应可明显改善心脏保存6h后心功能的恢复 ,减轻心肌酶的漏出 ,减轻缺血 再灌注损伤。且其分子基础是HSP72 ,其保护机制可能与内皮细胞保护有关更多还原

【Abstract】 ObjectiveHeat shock preconditioning model was used to investigate whether preconditioning can improve the myocardial recovery following long term cold arrest and its possible mechanims and molecular basis. MethodsTwenty healthy rabbits were randomly divided into two groups equally: group Ⅰas control group and group Ⅱ as heat shock pretreatment group. Before storage, the hearts were perfused with K H solution for 35?min, then arrested with STS (4?℃) and immersed in STS (4?℃) for storage for 6?h. The hearts were re perfused with 37?℃ K H solution for 25?min. Before storage and at the end of reperfusion, heart rate (HR), coronary flow (CF), left ventricular systolic pressure (LVSP) and left ventricular end diastolic pressure (LVEDP) were measured. The post storage recovery of cardiac function was expressed as a percentage of prestorage control values. The contents of HSP72, NO, CK MB, LDH, SOD, LPO in myocardial tissues were measured at the end of reperfusion. Myocardial water content was also measured at the same time. Results The myocardial recovery in the group Ⅱ was more satisfactory than in the group Ⅰ and correlated with the content of HSP72 in myocardial tissues (r= 0.95). The content of NO in myocardial tissue in the group Ⅱ was obviously higher than in the group Ⅰ. Conclusions Heat shock preconditioning could obviously improve the myocardial recovery in the heart after long term cold storage for 6?h, reduce the enzymes release and the ischemia/reperfusion injury. HSP72 was responsible for the molecular basis of heat shock preconditioning.The protective effect of HSP72 might be induced by endothelia protection.更多还原