运动心脏内分泌功能可复性的研究

为了进一步探讨运动心脏的可复性及其与病理心脏的本质差异，通过动物实验模拟运动心脏，观察了停止运动训练８周后心脏重量的变化，并对心肌组织与血浆中心钠素和降钙素基因相关肽含量进行了放射免疫测定。结果显示，经过１２周耐力训练后，心脏重量指数显著增高５１％；心房肌组织与血浆中心钠素含量分别显著增高４９％和７９％；心房肌组织与血浆中降钙素基因相关肽含量分别显著增高３６％和１９％。停止训练８周后，心脏重量指数较训练时显著降低２４％，心脏绝对重量和心脏重量指数与其对照组无显著差异；心房肌组织与血浆中心钠素含量分别较训练时显著降低２２％和３３％，基本恢复到正常对照水平；心房、心室肌组织与血浆降钙素基因相关肽含量分别较训练时降低１７％、８％和３％，也恢复到正常对照水平。研究结果表明，运动心脏确有心肌肥大，同时，运动心肌组织，尤其心房组织中心钠素和降钙素基因相关肽的产生与分泌水平增高，对运动性心肌肥大的发生、心肌收缩性的增强及冠脉循环的改善起重要调节作用。停训后运动心肌细胞心钠素和降钙素基因相关肽的改变不仅表明运动心脏内分泌功能改变具有可复性，而且，进一步证实运动心脏与病理心脏有着本质的差别。

The Reversibility of Cardiac Endocrine Function in Deconditioned Rats

In order to investigate the reversibility of exercise induced heart remodeling and the differences with pathological heart,the changes of myocardial and plasma atrial natriuretic factor(ANF) and calcitonin gene related peptide(GCRP) were determined by radioimmunoassays.40 male SD rats were randomly divided into endurance running group,deconditioning group and their sedentary controls.The results showed that,after trainning,the heart weight to body weight ratio was significantly increased 51%;the contents of atrial and plasma ANF significantly increased 49% and 79%,respectively,as compared with their controls(p<0.05);the contents of atrial and plasma GCRP significantly increased 36% and 19%,respectively,as compared with their controls(P<0.05).After deconditioning,the heart weight to body weight ratio was significantly decreased 24% as compared with the training group(P<0.05);the contents of atrial and plasma ANF decreased 22% and 33%,respectively,as compared with the training group(P<0.05);the contents of atrial,ventricular and plasma GCRP decreased 17%,8% and 3%,respectively,as compared with the training group,and there were no significant differences with their controls.The results suggested that there was a cardiac hypertrophy after endurance training.The training adaptation of myocardial and circulatory ANF and GCRP was reversible while deconditioning,and it was the essential difference between exercise induced cardiac hypertrophy and patholological cardiac hypertrophy.