运动性疲劳状态下大鼠心肌线粒体内钙、MDA及磷脂酶A-2的变化

主要目的：为了研究运动性疲劳状态下心肌组织损害的变化规律。方法：以SD大鼠递增负荷急性力竭跑台运动为疲劳模型，应用形态学手段和分子生化技术，分别测定了运动后两组大鼠即刻心肌线拉体内钙含量、脂质过氧化反应产物内二醛（HDA）、谷胱甘肽过氧化物酶（GSH—px）、超氧化物歧化酶（SOD）、心肌组织匀浆内酸性磷酸酶（Acid Phosphatase，ACP）和β葡萄糖醛酸酶（Beta—glucuronidase），磷脂酶A2（PIA2）等指标做了定位和定量研究。结果表明，第4周末，一般训练组和力竭训练组大鼠心肌线粒休内钙含量、MDA和GSH—px、SOD、PLA2活性和心肌ACP、β-葡萄糖醛酸酶的活性未见异常改变（P〉0．05）。但是第8周末，力竭训练组心肌线粒体内钙、MDA含量和PLA2活性明显升高，GSH含量和SOD活性明显降低；第8周末，心肌ACP和β-葡萄糖醛酸酶明显增加。结论：运动性状态下心肌线粒体的结构和功能发生了明显变化，这些变化可能是引起疲劳状态下心肌损伤的主要原因。

The Change of the Myocardial Acid Phosphatase,Beta-glucuronidase,and the Mitochondrial Ca,MDA,PLA2 in Rat Heart during Exhaustive Exercise

Rats running with an incremental intensity to exhaustion were used as an experimental model.The experiment was designed to determine the change of prepared mitochondrial immediately after exhaustive exercise.To investigate the change of exhaustive exercise on the myocardial acid phosphatase,beta-glucuronidase.and the mitochondrial Ca,MDA,PLA2electron microscope technique were used in exhaustive exercise group(EG)and control group(CG)rats.There was no abnormal changes on the myocardial acid phosphatase,beta-glucuronidase,and the mitochondrial Ca.MDA,PLA2in EG and CG at the end of4weeks(P>0.05),but the mitochondrial Ca,MDA content and beta-glucuronidase and myocardial acid phosphatase and the mitochondrial Ca,MDA.PLA2activites were increased signficantly and the GSH-px,SOD activites was decreased significantly in EG at the eng of8weeks(P<0.01).The results indicated that the myocardial was damaged,it is concluded that exhaustive exercise could exert change on the myocardial and myocardial mitochondrial.