中文摘要：

目的通过制备小鼠机械性创伤模型，观察过氧亚硝基（ONOO-）在机械性创伤致心肌细胞凋亡中的作用和机制。方法利用Noble-Collip创伤仪制作非致死性小鼠创伤模型，通过比色法测定心肌组织caspase3活性，TUNEL染色观察心肌细胞凋亡指数，化学发光法检测总一氧化氮（NOx）含量，EIJSA方法检测心肌组织中过氧亚硝基标志物硝基酪氨酸（Nitrotyrosine，NT）含量。结果机械创伤小鼠心肌组织中发生明显的细胞凋亡，同时心肌组织中一氧化氮含量和硝基酪氨酸含量均增高。结论过氧亚硝基造成的心肌组织蛋白质硝基化是机械创伤致心肌细胞凋亡的重要机制，减少过氧亚硝基的生成有助于减轻机械创伤后心肌损伤。

英文摘要：

Objective To determine whether peroxynitrite （ONOO-） contribute to posttraumatic cardiomyocyte apoptosis, and if so, to investigate the mechanisms involved. Methods Male adult mice were subjected to nonlethal traumatic injury by Modified Noble-Collip drum. Cardiomyocyte apoptosis was determined by measurement of caspase 3 activity and TUNEL staining. Cardiac production of total nitric oxide and nitryrosine were determined by chemiluminescent method and ELISA, respectively. Results Cardiomyocyte apoptosis gradually increased and reached a maximal level 12 h after trauma. In the traumatized hearts, nitric oxide was significantly increased. Moreover, a highly cytotoxic reactive species, peroxynitrite, was markedly increased in the traumatic heart, and there was a significant positive correlation between cardiac nitrotyrosine content and caspase 3 activity. Conclusion Nonlethal traumatic injury caused apoptotic cardiomyocyte death, in which peroxynitrite resulting in nitration of cardiac tissue played an important role.