摘要
目的观察模拟失重大鼠心肌细胞间缝隙连接蛋白CX43表达量及分布的变化 ,探讨该状态下易于发生心律失常的部分机制。方法将成年雄性Wistar大鼠 1 6只 ,随机分为正常对照组及尾部悬吊 30°模拟失重 2周组 ,应用免疫组化、WesternBlot、电子透射电镜检测大鼠心肌组织间连接蛋白CX43的表达、分布变化及缝隙连接超微结构的改变。结果与对照组相比 ,模拟失重组CX43表达量明显减少 (P <0 .0 5 ) ,并出现分布紊乱 :横向侧缝连接占总连接比例增加 (P <0 .0 5 ) ,电镜扫描显示 ,部分缝隙连接间隙消失。结论模拟失重可引起大鼠心肌间CX43表达减少及分布紊乱 ,从而可能改变心肌细胞间传导速度及途径 ,易于出现传导阻滞及折返 ,诱发心律失常。
Objective To observe the expression and distribution changes of connexin 43(CX) in rats' myocardium after simulated microgravity and explore the partial mechanism of arrhythmia. Method Male Wistar rats were randomly assigned to either tail-suspension group(SUS) or control group(CON). Immunohistochemistry and Western Blot were used to detect the expression and the distribution of CX43. Electromicroscope was used to observe the ultrastructural changes. Result In SUS group, the decrease of CX43 and the distribution disturbance were obvious (P<0.05), the proportion of the side-to-side gap junction increased(P<0.05),and space between some gap junctions disappeared. Conclusion The results show that CX43 decreased significantly and distributed irregularly after simulated microgravity . These can cause the changes of cardiac electric conduction velocity and direction. As a result, conduction block and reentry may occur. And these might be the partial mechanism of cardiac arrhythmia.
出处
《航天医学与医学工程》
CAS
CSCD
北大核心
2003年第6期448-451,共4页
Space Medicine & Medical Engineering
基金
中国载人航天工程基金资助
关键词
失重模拟
心肌
心律失常
缝隙连接
CX43
weightlessness simulation
myocardium
arrhythmia
gap junction
CX43