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目的:探讨一次力竭和反复力竭运动后大鼠心传导组织窦房结(SAN)、房室交界区(AJ)的组织结构及连接蛋白40(Connexin 40,Cx40)表达的时相性变化和规律。方法:健康成年雄性SD大鼠90只,分为一次力竭游泳组、反复力竭游泳组及安静对照组。游泳组分别于力竭后即刻、6小时、12小时、24小时取材。采用HE、Msson及免疫组织化学染色和图像分析法,观察大鼠SAN、AJ组织结构及其Cx40的表达。结果:一次力竭和反复力竭两种力竭运动后大鼠SAN、AJ组织出现缺血缺氧和胶原纤维增生等改变;Cx40在力竭运动后失去原有的规律分布,由胞膜转移至胞浆,Cx40积分光密度值有所降低,6小时时降低最为显著(P<0.01)。结论:一次力竭运动和反复力竭运动可导致心脏窦房结、房室交界区组织结构缺血缺氧性改变,Cx40不仅表达减少,其分布模式等缝隙连接结构功能也发生异常改变,是急性大强度运动后心律失常与心肌微损伤发生的重要机制。
OBJECTIVE: To investigate the histological structure and connective tissue protein 40 (Cx40) expression in the sinoatrial node (SAN) and atrioventricular junction (AJ) of rats after exhaustive exercise and exhaustive exhaustive exercise law. Methods: 90 healthy adult male Sprague-Dawley rats were divided into one exhaustive swimming group, repeated exhaustive swimming group and quiet control group. Swimming group were exhausted immediately after 6 hours, 12 hours, 24 hours drawing. HE, Msson and immunohistochemical staining and image analysis were used to observe the tissue structure and the expression of Cx40 in SAN and AJ rats. Results: After exhaustive exercise and exhaustive exhaustive exercise, the changes of ischemia and hypoxia and collagen fiber hyperplasia were observed in SAN and AJ tissues of rats. Cx40 lost its regular distribution after exhaustive exercise, To the cytoplasm, Cx40 integral optical density value decreased, the most significant reduction at 6 hours (P <0.01). CONCLUSION: A single exhaustive exercise and repeated exhaustive exercise can lead to alteration of ischemia-reoxygenation in cardiac sinus node and atrioventricular junctional area. Not only the expression of Cx40 but also the abnormal distribution of Cx40 are also changed Acute high intensity exercise arrhythmia and myocardial micro injury occurs after the important mechanism.