急性疲劳运动对大鼠心血管超微结构及血管功能的影响

目的观察急性疲劳运动对大鼠心血管超微结构及血管功能的影响。方法 24只雄性Wistar-Kyoto大鼠接受适应性训练5d后,分为安静对照组（不运动）、适应训练组（维持适应性训练的运动量,连续运动5d）和急性疲劳运动组（疲劳运动5d,直至出现明显拒跑）,每组8只。运动结束后,检测各组大鼠主动脉收缩与舒张功能;透射电子显微镜观察主动脉和心肌组织超微结构变化。结果与安静对照组和适应训练组比较,急性疲劳运动组大鼠主动脉对高钾溶液诱导的血管收缩反应无明显变化,对苯肾上腺素引起的收缩反应显著减弱（P〈0.01）;对乙酰胆碱诱导的内皮依赖性血管舒张反应明显增强（P〈0.01）,给予一氧化氮合酶阻断剂干预后血管舒张反应完全被抑制。透射电子显微镜观察显示,急性疲劳运动组大鼠主动脉内膜内皮细胞损伤,内弹力膜断裂,平滑肌细胞层单核-巨噬细胞浸润;心肌纤维收缩带形成,线粒体变性。结论疲劳运动可导致心肌线粒体及血管内膜损伤;血管收缩减弱,舒张呈增强趋势,可能是过度运动后发生低血压及猝死的原因之一。

Effects of acute exhaustive running on rat cardiovascular ultrastructure and vessel function

Objective To observe the effects of acute exhaustive running on rat cardiovascular ultrastructure and vessel function. Methods After adaptative running for 5 d, 24 male Wistar-Kyoto rats were assigned to sedentary control group (no more running, n=8), adaptative running group (adaptative running for another 5 d, n=8) and acute exhaustive running group (exhaustive running for another 5 d till refusal to running, n=8). After the end of running, the contraction and relaxation function of aortic vessels were assessed, and the ultrastructure of myocardium and aorta was examined under transmission electron microscope. Results Compared with sedentary control group and adaptative running group, the aortic contraction response to high potassium was not altered, while that to phenylephrine was significantly depressed in acute exhaustive running group (P<0.01). The endothelium-dependent vessel relaxation to acetylcholine was significantly enhanced in acute exhaustive running group (P<0.01), and was blocked by nitric oxide synthase inhibitor. Lysis of aortic endothelium, break of internal elastic lamina, infiltration of mononuclear macrophages around smooth muscles, degeneration in mitochondria and contraction band in myocardium in acute exhaustive running group were revealed by transmission electron microscopy. Conclusion Acute exhaustive running could lead to the impairment of vessel wall and myocardial mitochondria. The improvement in vessel relaxation and depression in contraction response may contribute to hypotension and sudden death after overexercise.