摘要
结扎实验犬左冠状动脉前降支45min后开放45min,以造成心肌缺血和再灌注模型。观察缺血和再灌注期心肌丙二醛含量和超微结构的变化。发现在缺血期心肌丙二醛有增加,但不显著,超微结构损伤较轻;在再灌注期,丙二醛显著增加,超微结构损害严重,提示氧自由基主要产生于再灌注期,是心肌再灌注损伤的重要原因。
Dog models of myo- cardial ischemia and reperfusion were made by ligating the left anterior decending coronary artery for 45 min, and reperfusing for 45 min. Malon dialdehyde (MDA) and ultrastructure changes in myocardium were investigated during ischemia and reperfusion. Insignificant increase of myocardial MDA and comparatively slight damage of myocardial ultrastructure were observed in the ischemic period; significant increase of myocardial MDA and severe damage of myocardial ultrastructure were found in the reperfusion period, suggesting that myocardial oxygen free radicals (responsible for myocardial injury) are produced primarily during reperfusion
出处
《宁夏医学杂志》
CAS
1993年第2期75-77,共3页
Ningxia Medical Journal
关键词
丙二醛
超微结构
心肌
氧
自由基
Malondtaldehyde/anal
Spectrometry,fluorescence
Microscopy,electron /ultrastruct
Ischemia/experimental study
Perfusion/experimental study Myocardium/ inj
Dogs
Oxygen free radicals
