凋亡在机械性创伤致继发性心肌损伤中的作用  

Role of apoptosis in secondary heart injury induced by mechanical trauma

作　　者：李秀荣 燕子[2] 闫莉[2] 郭丽[2] 王瑾[2] 梁峰[3] 

机构地区：[1]山西电力职业技术学校基础部,太原市030021 [2]山西医科大学基础医学院生理教研室 [3]山西医科大学附属太钢总医院胸心外科

出　　处：《中国心血管病研究》2009年第3期204-206,共3页Chinese Journal of Cardiovascular Research

基　　金：国家自然科学基金（30872680）

摘　　要：目的通过制备大鼠机械性创伤模型，探讨心肌细胞凋亡在机械性创伤致继发性心功能损伤中的作用。方法利用Noble—Collip创伤仪制备非致死性大鼠创伤模型，通过TUNEL染色和DNAladder检测心肌细胞凋亡情况，使用LVDP、±dP／dtmax来判定心脏功能。结果机械性创伤时心功能显著下降，心肌细胞发生明显的凋亡，给予caspase抑制剂，大鼠心功能损伤降低。结论心肌细胞凋亡是导致创伤时继发性心功能损伤的重要机制，抗凋亡治疗有望成为临床减轻这种心肌损伤的一种新的措施。Objective To determine the role of myocardial cell apoptosis in secondary heart injury induced by mechanical trauma in mechanical trauma rat model. Methods Noble-Collip drum was used to establish nonlethal traumatic rat model. Cardiocyte apoptosis was determined by TUNEL staining and the formation of DNA ladder. Cardiac function was assessed by left ventricular diastolic pressure （LVDP）, maximal positive and negative values of the instantaneous first derivative of LVP （＋dP/dtmax and -dP/dtmax）. Results Mechanical trauma resulted in significant cardiomyocyte apoptosis and decrease of cardiac function. Treatment with caspase inhibitor obviously depressed the damage of cardiac function. Conclusion Cardiocyte apoptosis contributes to post-trauma cardiac dysfunction. Antiapoptotic treatment might be a novel strategy in reducing post-trauma cardiac dysfunction.

关 键 词：凋亡 创伤 心脏损伤 

分 类 号：Q95-33[生物学—动物学] R542.2[医药卫生—心血管疾病]