Recuperative Potential of Cardiac Muscle following Relief of Pressure Overload Hypertrophy and Right Ventricular Failure in the Cat
Recuperative Potential of Cardiac Muscle following Relief of Pressure Overload Hypertrophy and Right Ventricular Failure in the Cat
复制标题
猫压力超负荷肥大和右心室衰竭缓解后心肌的恢复潜力
DOI：
10.1161/01.res.40.1.41
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发表时间：
1977
影响因子：
20.1
通讯作者：
J. Spann
中科院分区：
文献类型：
--
作者：
R. Coulson;S. Yazdanfar;E. Rubio;A. Bove;G. Lemole;J. Spann
摘要本研究检查了猫心脏的恢复潜力，实验性右心室压力超负荷（10至14天），引起肥厚伴或不伴充血性心力衰竭。研究了五组猫：正常对照组，一组肺动脉收缩70%，产生右心室肥大（RVH），一组收缩87%，也产生右心室肥大，但伴有充血性心力衰竭（CHF）;和两组类似地经受压力超负荷，但在缓解压力后允许30天的恢复期。压力过载70%和87%的肺动脉收缩均与广泛的右心室肥大、心肌收缩功能抑制和心脏去甲肾上腺素储备严重减少相关（正常，1.42 g/g：RVH，0.11 g/g; CHF，0.01 g/g）。在肺动脉收缩缓解30天后，血流动力学功能恢复正常。在RVH缓解的猫中，右心室重量和收缩功能正常，但儿茶酚胺耗竭持续存在。CHF缓解的猫表现出收缩功能抑制和心肌去甲肾上腺素耗竭，右心室重量没有恢复正常。所有压力超负荷未缓解心脏的心肌均表现出缩短速度降低和负荷维持能力降低。单独使用RVH的猫在缓解后恢复了正常的肌肉缩短速度和承重能力。然而，CHF缓解组的心肌仅恢复了无负荷缩短速度，而维持负荷的能力仍然受到抑制。我们的结论是，如果没有发生充血性心力衰竭，压力超负荷损伤的心肌的恢复潜力是足够的。心力衰竭会导致心肌产生力的能力持续下降。由于压力超负荷引起的肥大（伴或不伴CHF）导致心脏儿茶酚胺耗竭，这不容易通过缓解超负荷而逆转。
SUMMARY. This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe reduction of cardiac norepinephrine stores (normal, 1.42 &mgr;g/g: RVH, 0.11&mgr;g/g; CHF, 0.01 &mgr;g/g)-After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.