烧伤延迟复苏诱导心肌细胞凋亡

目的 探讨烧伤延迟复苏能否引起心肌细胞凋亡及其发生机制。方法 30％Ⅲ度烧伤6h后进行复苏，再灌注2、10、18h后抽提心肌组织中基因组DNA，用PCR试剂盒检测凋亡，PCR产物行琼脂糖凝胶电泳，观察基因组DNA是否出现特征性的凋亡图像并观察心肌组织中一氧化氮(NO)和脂肪酸含量的变化。结果烧伤延迟复苏后心肌组织基因组DNA出现标志凋亡的“梯形”图像，随延迟复苏时间的延长大鼠心肌组织凋亡的发生率增加。NO在延迟复苏后2h显降低，延迟复苏后不饱和脂肪酸含量显低于烧伤后立即复苏大鼠，细胞膜僵硬度显增加。结论烧伤后延迟复苏导致心肌组织细胞凋亡，其发生与NO含量减少、氧自由基产生增加有关。

Myocardial apoptosis induced by delayed fluid resuscitation in a burned rat model

OBJECTIVE: To explore the possibility and the mechanism of myocardial apoptosis induced by delayed fluid resuscitation in a burned rat model and its relationship with nitric oxide (NO) and oxygen-derived free radicals. METHODS: In a rat model with 30% III degree burn, the genomic DNA of the myocardial tissue was detected with ApoAlert(TMLM)-PCR Ladder Assay Kit and visualized with agarose gel electrophoresis. Meanwhile, the NO and the content of unsaturated fatty acids were measured. RESULTS: In rats receiving delayed fluid resuscitation following burn, the myocardial genomic DNA exhibited DNA ladder-index of apoptosis, and the contents of myocardial NO and unsaturated fatty acid were much lower than those in rats receiving immediate resuscitation (P < 0.05). CONCLUSION: The myocardial tissue undergoes apoptosis in burned rats receiving delayed fluid resuscitation, and the decreased NO and the production of oxygen-derived free radicals are also observed in this process.