Mocanu M M, Steare S E, Evans M C, Nugent J H, Yellon D M
Victor Babes Institute, Bucharest, Romania.
Free Radic Biol Med. 1993 Oct;15(4):459-63. doi: 10.1016/0891-5849(93)90046-w.
Prior heat stress leads to an enhancement of postischemic mechanical function and improvement in biochemical indices of injury in the rat heart, associated with an elevation in endogenous catalase activity. We have examined the effect of heat stress on free radical release during reperfusion in the isolated rat heart using electron spin resonance (ESR). Twenty four hours after heat stress or sham treatment, hearts were perfused in the Langendorff mode and subjected to 10 min of no-flow global ischemia followed by 10 min of reperfusion. Coronary effluent was collected at specific time points in PBN for ESR measurement. A PBN adduct was identified with characteristics consistent with an alkoxyl radical: PBN-LO. In sham hearts there was a rapid rise in adduct release to a maximum (228 +/- 15% of stabilization values, p < .05) occurring 1 min into reperfusion. In heat stress hearts there was no significant rise in adduct release during the reperfusion period. Pretreatment of hearts with 3-amino triazole, an inhibitor of catalase, failed to clarify whether the protection seen in heat stress hearts was a result of the elevation in catalase activity. These results suggest that heat stress protects the myocardium against the oxidative stress of ischemia-reperfusion.
预先的热应激可使大鼠心脏缺血后的机械功能增强，损伤的生化指标得到改善，这与内源性过氧化氢酶活性升高有关。我们使用电子自旋共振（ESR）研究了热应激对离体大鼠心脏再灌注期间自由基释放的影响。热应激或假手术处理24小时后，心脏以Langendorff模式灌注，进行10分钟无血流全心缺血，随后再灌注10分钟。在特定时间点收集冠状动脉流出液于PBN中用于ESR测量。鉴定出一种PBN加合物，其特征与烷氧基自由基一致：PBN-LO。在假手术心脏中，加合物释放在再灌注1分钟时迅速上升至最大值（稳定值的228±15%，p<.05）。在热应激心脏中，再灌注期间加合物释放没有显著上升。用过氧化氢酶抑制剂3-氨基三唑预处理心脏，未能明确热应激心脏中观察到的保护作用是否是过氧化氢酶活性升高的结果。这些结果表明，热应激可保护心肌免受缺血-再灌注的氧化应激。
