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首页> 外文期刊>American Journal of Physiology >Mechanical traumatic injury without circulatory shock causes cardiomyocyte apoptosis: role of reactive nitrogen and reactive oxygen species.
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Mechanical traumatic injury without circulatory shock causes cardiomyocyte apoptosis: role of reactive nitrogen and reactive oxygen species.

机译：没有循环休克的机械性外伤会导致心肌细胞凋亡：活性氮和活性氧的作用。

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摘要

Apoptotic cell death plays a critical role in tissue injury and organ dysfunction under a variety of pathological conditions. The present study was designed to determine whether apoptosis may contribute to posttraumatic cardiac dysfunction, and if so, to investigate the mechanisms involved. Male adult mice were subjected to nonlethal traumatic injury, and cardiomyocyte apoptosis, cardiac function, and cardiac production of reactive oxygenitrogen species were determined. Modified Noble-Collip drum trauma did not result in circulatory shock, and the 24-h survival rate was 100%. No direct mechanical traumatic injury was observed in the heart immediately after trauma. However, cardiomyocyte apoptosis gradually increased and reached a maximal level 12 h after trauma. Significantly, cardiac dysfunction was observed 24 h after trauma in the isolated perfused heart. This was completely reversed when apoptosis was blocked by administration of a nonselective caspase inhibitor immediately after trauma. In the traumatized hearts, reactive nitrogen species (e.g., nitric oxide) and reactive oxygen species (e.g., superoxide) were both significantly increased, and maximal nitric oxide production preceded maximal apoptosis. 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. Our present study demonstrated for the first time that nonlethal traumatic injury caused delayed cell death and that apoptotic cardiomyocyte death contributes to posttrauma organ dysfunction. Antiapoptotic treatments, such as blockade of reactive nitrogen oxygen species generation, may be novel strategies in reducing posttrauma multiple organ failure.
机译：在多种病理条件下，凋亡性细胞死亡在组织损伤和器官功能障碍中起着关键作用。本研究旨在确定凋亡是否可能导致创伤后心脏功能障碍，如果是，则调查所涉及的机制。雄性成年小鼠遭受非致命性创伤，并测定了心肌细胞的凋亡，心脏功能和活性氧/氮物质的心脏产生。改良的Noble-Collip鼓损伤未导致循环休克，其24小时生存率为100％。创伤后立即在心脏内未观察到直接的机械创伤。然而，心肌细胞凋亡在创伤后12小时逐渐增加并达到最高水平。明显地，在离体的灌注心脏中，创伤后24小时观察到心脏功能障碍。当创伤后立即通过给予非选择性胱天蛋白酶抑制剂阻断凋亡，这完全被逆转。在受创伤的心脏中，反应性氮（例如一氧化氮）和反应性氧（例如超氧化物）都显着增加，并且一氧化氮的最大产生先于最大的细胞凋亡。此外，在创伤性心脏中，具有高度细胞毒性的反应性物种过氧亚硝酸盐显着增加，并且心脏硝基酪氨酸含量与caspase 3活性之间存在显着的正相关。我们的研究首次证明了非致命性外伤导致细胞死亡延迟，而凋亡性心肌细胞死亡导致创伤后器官功能障碍。抗凋亡治疗，例如阻断活性氮氧的产生，可能是减少创伤后多器官衰竭的新策略。

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