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不同强度运动后大鼠心肌细胞和血浆中心房钠尿肽的变化

Alterations of atrial natriuretic peptide in cardiomyocytes and plasma of rats after different intensity exercise.

作者信息

Pan S S

机构信息

Department of Sports Anatomy, College of Exercise and Sport Science, Shanghai University of Sport, Shangai, China.

出版信息

Scand J Med Sci Sports. 2008 Jun;18(3):346-53. doi: 10.1111/j.1600-0838.2007.00684.x. Epub 2007 Jun 6.

Abstract

To characterize the effect of long-term exercise training at different intensities on endocrine structure and function of the heart, plasma atrial natriuretic peptide (ANP) levels, expression of ANP in cardiomyocytes, and ultrastructure of cardiomyocytes were examined by radioimmunoassay, immunohistochemistry and transmission electron microscopy in Sprague-Dawley rats trained on a treadmill at different intensities for 8 weeks. The plasma ANP increased gradually with increasing exercise intensity. The immunoreactivity of ANP in cardiomyocytes increased in the moderate- and high-intensity exercise group and decreased in the exhaustive exercise group. The ANP electron-dense granules and the quantity and volume of mitochondria increased in moderate and high-intensity exercise group. The ANP electron dense granules decreased and the mitochondria tumefied in the exhaustive exercise group. The changes of plasma ANP have a tendency of increasing gradually with increase in exercise intensity. Moderate and high-intensity exercise increases ANP synthesis and storage in cardiomyocytes and induces adaptive changes in the ultrastructure of cardiomyocytes. The decrease of ANP immunoreactivity in cardiomyocytes after exhaustive exercise is probably the result of massive depletion and induces damaging changes in the ultrastructure of cardiomyocytes.

摘要

为了阐明不同强度的长期运动训练对心脏内分泌结构和功能的影响,采用放射免疫分析法、免疫组织化学法和透射电子显微镜法,对在跑步机上以不同强度训练8周的Sprague-Dawley大鼠的血浆心钠素(ANP)水平、心肌细胞中ANP的表达以及心肌细胞超微结构进行了检测。血浆ANP水平随运动强度增加而逐渐升高。中、高强度运动组心肌细胞中ANP的免疫反应性增加,力竭运动组则降低。中、高强度运动组ANP电子致密颗粒以及线粒体的数量和体积增加。力竭运动组ANP电子致密颗粒减少,线粒体肿胀。血浆ANP的变化有随运动强度增加而逐渐升高的趋势。中、高强度运动增加心肌细胞中ANP的合成与储存,并诱导心肌细胞超微结构发生适应性改变。力竭运动后心肌细胞中ANP免疫反应性降低可能是大量消耗的结果,并导致心肌细胞超微结构发生损伤性改变。

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