Chronic swimming reverses cardiac dysfunction and myosin abnormalities in hypertensive rats.
Chronic swimming reverses cardiac dysfunction and myosin abnormalities in hypertensive rats.
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慢性游泳可逆转高血压大鼠的心脏功能障碍和肌球蛋白异常。
DOI：
10.1152/jappl.1986.60.4.1435
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Scheuer,J
中科院分区：
文献类型：
--
作者：
Schaible,TF;Malhotra,A;Ciambrone,GJ;Scheuer,J
本研究的目的是确定慢性游泳计划是否可以逆转肾性高血压大鼠心脏中发现的心脏功能下降和肌球蛋白生物化学改变。在高血压发病后10周[中点（m）]，在离体工作心脏装置中研究了正常血压对照组（C）和高血压组（H）的心脏，并分析了肌球蛋白生物化学。一半的对照组和高血压组动物进行为期10周的游泳训练，并将其心脏与年龄匹配的久坐大鼠进行比较。Cm和Hm之间研究中点时的体重或Ce、Swe、He或H-Swe之间研究终点（e）时的体重无差异。游泳对血压正常或高血压大鼠的血压均没有影响。干心脏重量增加了46%，在Hm相比，Cm和36%，在他，21%，在Swe，和61%，在H-Swe相比，铈。在中期和终点研究中，高血压与冠状动脉流量、每克左心室每搏作功、射血分数和中壁缩短分数降低相关。此外，肌动蛋白激活的肌球蛋白腺苷三磷酸酶（ATP酶）的活性下降，在Hm和他与V3肌球蛋白同工酶的含量增加。虽然H-Swe的冠状动脉功能不全没有得到纠正，但与对照心脏相比，每搏作功、射血分数和壁中部缩短分数均正常化。肌球蛋白ATP酶活性和肌球蛋白同工酶分布在H-Swe中同样恢复。（250字处删节）
The purpose of this study was to determine whether a chronic swimming program could reverse the decreased cardiac function and altered myosin biochemistry found in hearts of rats with established renal hypertension. Ten wk after the onset of hypertension [midpoint (m)], hearts from normotensive controls (C) and hypertensives (H) were studied in an isolated working heart apparatus, and myosin biochemistry was analyzed. Half of the control and hypertensive animals were then subjected to a 10-wk swimming program (Sw) and their hearts were compared with those from age-matched sedentary rats. Body weight was no different at the midpoint of the study between Cm and Hm or at the end point (e) of the study among Ce, Swe, He, or H-Swe. Swimming had no effect on blood pressure in either normotensive or hypertensive rats. Dry heart weight was increased by 46% in Hm compared with Cm and by 36% in He, 21% in Swe, and 61% in H-Swe when compared with Ce. Hypertension was associated in both the mid- and end-point studies, with decreases in coronary flow, stroke work (both per gram left ventricle), ejection fraction, and midwall fractional shortening. In addition, actin-activated myosin adenosinetriphosphatase (ATPase) activity was decreased in Hm and He associated with an increase in the content of the V3 myosin isoenzyme. Although the coronary deficit was not corrected in H-Swe, stroke work, ejection fraction, and fractional midwall shortening were normalized compared with control hearts. Myosin ATPase activity and the myosin isoenzyme distribution were similarly restored in H-Swe.(ABSTRACT TRUNCATED AT 250 WORDS)