Zhang Jiaping, Huang Yuesheng, Zhou Xin, Liu Jing, Luo Zhonghua, Yang Zongcheng
Institute of Burn Research, Southwestern Hospital, The Third Military Medical University, Chongqing 400038, P.R. China.
Zhonghua Shao Shang Za Zhi. 2002 Oct;18(5):272-5.
To investigate relationship between apoptosis of the cardiac myocytes and myocardial dysfunction in severely scalded rats.
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.
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.
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.
