严重烫伤大鼠心肌细胞凋亡与心功能损害的关系  

The relationship between apoptosis of the cardiac myocytes and myocardial dysfunction in severely scalded rats

作　　者：张家平[1] 黄跃生[1] 周新[1] 刘敬[1] 罗中华[1] 杨宗城[1] 

机构地区：[1]第三军医大学西南医院全军烧伤研究所,重庆400038

出　　处：《中华烧伤杂志》2002年第5期272-275,共4页Chinese Journal of Burns

基　　金：国家杰出青年科学基金资助项目 ( 3 0 12 5 0 40 ) ;国家重点基础研究发展规划资助项目 (C19990 5 42 0 2 );全军医药卫生科研基金课题资助项目 ( 0 1L0 66);高等学校骨干教师资助计划资助项目

摘　　要：目的　观察大鼠烫伤后早期心肌细胞凋亡规律 ,探讨细胞凋亡与心功能损害的关系。方法　Wistar大鼠 4 0 %TBSAⅢ度烫伤。伤后不同时相点 ,取左室心肌组织切片 ,采用DNA切口末端标记法 [termialdeoxynucleotibyltransferase(TdT) mediateddUTP biotinnickendlabeling ,TUNEL]染色和左室心肌组织Caspase 3活性双指标联合检测细胞凋亡 ,以四道生理记录仪监测左心室最大收缩压、左心室舒张末压和左室压力最大上升 /下降速率变化 ,测定心肌组织髓过氧化物酶 (MPO)、超氧化物歧化酶 (SOD)。　结果　烫伤后 6h ,大鼠心肌细胞TUNEL染色阳性 ,伤后 12h达高峰 ;Cas pase 3活性变化早于凋亡形态学变化 ,于伤后 3、6h达峰值 ;烫伤后大鼠左心功能包括收缩 /舒张功能明显受损 ,伤后 12h降至最低水平 ;心肌组织MPO活性增强伴SOD活性下降。　结论　心肌细胞凋亡是烫伤后大鼠心功能损害的原因之一 ,Caspase 3途径可能参与了凋亡过程 ,推测凋亡的诱导与中性粒细胞浸润。Objective To investigate relationship between apoptosis of the cardiac myocytes and myocardial dysfunction in severely scalded rats. Methods Wistar rats inflicted by 40% TBSA Ⅲ degree scalding were employed as the model. The myocardial tissue was obtained from the left ventricle at different postburn time points. Apoptosis was determined by the determination of myocardial tissue Caspase 3 activity and TUNEL staining (terminal deoxynucleotidyl transferase (TdT) mediated dUTP biotin nick end labeling). The LVSP (left ventricular systolic pressure), LVEDP (left ventricular end diastolic pressure) and +dp/dtmax (the rate of the rise of left ventricular pressure) and dp/dtmax (the rate of the fall of left ventricular pressure) were all monitored by four channel physiological recorder. In addition, myocardial activities of MPO and SOD were detected. Results The TUNEL staining of rat myocardial cells was positive at 6 postburn hour (PBH) and reached top level at 12 PBH. The change in Caspase 3 activity was earlier than that of apoptotic morphology and reached peak values at 3 and 6 PBHs. The left ventricular function (systolic and diastolic function) was significantly impaired after the scalding and dropped to the lowest levels at 12 PBHs. The increase in myocardial tissue MPO activity was accompanied by the decrease in SOD activity. Conclusion Myocardial cellular apoptosis was one of the reasons of postburn myocardial injury in scalded rats. Caspase protease cascade pathway might be involved in the process of apoptosis, which suggested that the initiation of apoptosis was closely related to the infiltration of neutrophils and to the release of large amounts of oxygen free radicals in myocardial tissue. [

关 键 词：中性粒细胞 严重烫伤 大鼠 心肌细胞 细胞凋亡 心功能 氧自由基 

分 类 号：R644[医药卫生—外科学] R542.2[医药卫生—临床医学]