EFFECTS OF CHRONIC BETA-ADRENERGIC-BLOCKADE ON THE LEFT-VENTRICULAR AND CARDIOCYTE ABNORMALITIES OF CHRONIC CANINE MITRAL REGURGITATION
EFFECTS OF CHRONIC BETA-ADRENERGIC-BLOCKADE ON THE LEFT-VENTRICULAR AND CARDIOCYTE ABNORMALITIES OF CHRONIC CANINE MITRAL REGURGITATION
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DOI：
10.1172/jci117277
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发表时间：
1994-06-01
影响因子：
15.9
通讯作者：
CARABELLO, BA
中科院分区：
文献类型：
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作者：
TSUTSUI, H;SPINALE, FG;CARABELLO, BA
β -阻滞剂改善各种心肌病左心室功能障碍的机制归因于改善心肌收缩功能或改善β -肾上腺素能反应性。在这项研究中，我们检验了两个假设：(a)慢性β阻断会改善二尖瓣反流引起的左心室功能障碍，(b)这种作用的一个重要机制是改善心肌的先天收缩功能。对两组6只慢性重度二尖瓣反流犬进行研究。3个月后，两组均出现相似且明显的左心室功能障碍。然后，一组逐渐被阻断，而第二组在没有进一步干预的情况下继续观察。在未阻塞的组中，收缩功能仍然受到抑制。然而，在接受慢性β阻断治疗的组中，收缩功能明显改善。在没有受体刺激的情况下，从未阻塞的心脏中分离出来的心肌细胞的收缩力受到极大的抑制。然而，从β阻塞心室分离的心肌细胞的收缩性几乎正常。与这些数据一致，肌纤维密度高得多，阻断组为55 +/- 4%，未阻断组为39 +/- 2% (P < 0.01)；因此，在β阻断组中有更多的收缩元素产生力。我们的结论是慢性β阻断改善慢性实验性二尖瓣反流左心室功能。这种改善与分离的心肌细胞先天收缩功能的改善有关，这反过来又与收缩元件数量的增加有关。
The mechanism by which beta blockade improves left ventricular dysfunction in various cardiomyopathies has been ascribed to improved contractile function of the myocardium or to improved beta-adrenergic responsiveness. In this study we tested two hypotheses: (a) that chronic beta blockade would improve the left ventricular dysfunction which develops in mitral regurgitation, and (b) that an important mechanism of this effect would be improved innate contractile function of the myocardium.Two groups of six dogs with chronic severe mitral regurgitation were studied. After 3 mo both groups had developed similar and significant left ventricular dysfunction. One group was then gradually beta-blocked while the second group continued to be observed without further intervention. In the group that remained unblocked, contractile function remained depressed. However, in the group that received chronic beta blockade, contractile function improved substantially.The contractility of cardiocytes isolated from the unblocked hearts and then studied in the absence of beta receptor stimulation was extremely depressed. However, contractility of cardiocytes isolated from the beta-blocked ventricles was virtually normal. Consistent with these data, myofibrillar density was much higher, 55 +/- 4% in the beta-blocked group vs. 39 +/- 2% (P < 0.01) in the unblocked group; thus, there were more contractile elements to generate force in the beta-blocked group.We conclude that chronic beta blockade improves left ventricular function in chronic experimental mitral regurgitation. This improvement was associated with an improvement in the innate contractile function of isolated cardiocytes, which in turn is associated with an increase in the number of contractile elements.