中文摘要：

目的观察烧伤后早期一次大面积切痂对大鼠心肌损伤的改善状况，并探讨其分子机制。方法将66只SD大鼠随机分为非切痂组（30只）、切痂组（30只）与正常对照组（6只）。将前两组大鼠造成30％TBSAⅢ度烫伤（以下称烧伤，切痂组伤后20min切除全部焦痂组织），并于伤后l、3、6、12、24h（每时相点6只）检测大鼠心肌线粒体中腺苷三磷酸（ATP）含量、血清中肌钙蛋白I（TnI）含量以及心肌线粒体DNA（mtDNA）4．8kb大片段缺失情况。正常对照组大鼠不作处理，同样检测上述指标。结果（1）两致伤组大鼠心肌线粒体中ATP含量均有下降，但伤后1、6h切痂组该值分别为（0，90±0．27）、（0．66±0．19）μg／mg蛋白，较非切痂组的（0．74±0，18）、（0.46±0．21）μg／mg蛋白有显著改善（P〈0．05）。（2）与正常对照组比较，切痂组大鼠伤后1、3h血清中TnI含量变化不明显，但伤后1、3、6h与非切痂组比较差异有统计学意义（P〈0．05或0．01）。（3）非切痂组大鼠在伤后1、3、24h发生了mtDNA 4．8kb的部分或全部大片段缺失，切痂组大鼠仅在伤后1、12h发生缺失，且平均缺失率较非切痂组低。结论烧伤后早期一次大面积切痂能显著减轻伤后心肌受损程度，其机制可能与降低伤后早期心肌mtDNA缺失率有关。

英文摘要：

Objective To investigate the alleviation of myocadial injury of rats after early escharectomy en masse of severe burns , and to explore its molecular mechanism. Methods Totally 66 SD rats were randomly divided into normal control（ n = 6） , non-escharectomy（ NE, n = 30） and escharectomy（ E, n=30, with total escharectomy 20 minutes after burns ） groups. The rats in the NE and E groups were inflicted with 30% TBSA full-thickness scald. The content of ATP in mitochondria, troponin I （Tn I） in serum and 4.8- kb deletion of myocardial mitochondrial DNA（mtDNA） of the rats in each group were determined at 1,3,6, 12 and 24 post-scald hours（PSH）. Results （ 1 ） The content of ATP in myocardial mitochondria was decreased in both E and NE groups, but it was obviously increased at 1 and 6 PSH （0.90 ± 0. 27 μg/mg , 0.66±0.19 μg/mg） in E group when compared with those in NE group （0.74 ±0.18 μg/mg , 0.46 ± 0.21 μg/mg, P 〈0.05 ）. （2） There was no obvious change in the serum content of Tn I in E group at 1 and 3 PSH, but the respective content in 1,3 and 6 PSH was markedly lower than those in NE group（ P 〈 0.05 ）. （3） The 4.8 kb deletion of myocardial mtDNA was found at 1, 3, 24 PSH in NE group, while it was observed only at 1, 12 PSH in E group. The partial and whole deletion rate in E group was lower than that in NE group. Conclusion Early escharectomy en masse can significantly alleviate the myocardial injury after burns,which might be related to its effect in lowering the deletion rate of myocardial mtDNA at early postburn stage.