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作 者:顾长海[1]
机构地区:[1]南阳理工学院体育教学部,河南南阳473003
出 处:《河南大学学报(自然科学版)》2013年第2期181-185,共5页Journal of Henan University:Natural Science
基 金:河南省科技攻关项目(112102310694)
摘 要:本实验选取60只雄性Wistar大鼠作为实验对象,建立2型糖尿病动物模型.观察2型糖尿病后大鼠心脏收缩功能及结蛋白的变化,以及游泳训练干预对上述变化的影响及机制.结果显示:2型糖尿病后,大鼠心脏最大收缩期和舒张期压力变化速率(±dp/dtmax)水平均极显著性降低(P<0.01),左室射血分数(LVEF)显著性下降(P<0.05).心肌组织纤维分布不匀,心肌细胞排列紊乱.相对地,游泳训练可有效抑制±dp/dtmax水平降低(P<0.05),提高射血分数,抑制结蛋白表达升高.以上结果说明,糖尿病可造成心脏收缩功能异常及心肌结蛋白表达增多,游泳训练可明显降低结蛋白的表达并改善心功能.In this paper, 60 male Wistar rats were subjected to establishing a type of 2 diabetes animal model. Post-diabetes, cardiac contractile function, expression of desmin protein level, and betterments induced by AIT were evaluated. Results showed that the values of ± dp/dtmax of myocardial contractility parameters very significant decreased( P〈 0.01 ), left ventricular ejection fraction(LVEF) visibly declined( P 〈 0.05 ). Also, uneven distributed of myocardial tissue and deranged cadiocytes were also perceived in the animals of control group. In contrast, those adverse modifications could be partially reversed by swimming trairfing, such as upgraded values of ± dp/dtmax, augmented value of LVEF, decreased desmin protein expression. Those results indicating that diabetes can cause cardiac systolic dysfunction and myocardial abnormal desmin expression, which can be somewhat normalized by swimming training.
分 类 号:G804.2[文化科学—运动人体科学]
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