Coulson R L, Yazdanfar S, Rubio E, Bove A A, Lemole G M, Spann J F
Circ Res. 1977 Jan;40(1):41-9. doi: 10.1161/01.res.40.1.41.
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 redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/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.
本研究检测了经历实验性右心室压力过载（为期10至14天）的猫心脏的恢复潜力，该压力过载引发了伴有或不伴有充血性心力衰竭的心肌肥大。研究了五组猫：正常对照组；一组进行70%肺动脉缩窄，产生右心室肥大（RVH）；一组进行87%缩窄，同样产生右心室肥大但伴有充血性心力衰竭（CHF）；还有两组同样经历了压力过载，但在压力过载解除后给予30天的恢复期。70%和87%的肺动脉缩窄均伴有广泛的右心室肥大、心肌收缩功能降低以及心脏去甲肾上腺素储备严重减少（正常为1.42微克/克；RVH为0.11微克/克；CHF为0.01微克/克）。肺动脉缩窄解除30天后，正常血流动力学功能恢复。在RVH已缓解的猫中，右心室重量和收缩功能正常，但儿茶酚胺耗竭持续存在。CHF已缓解的猫表现出收缩功能降低和心肌去甲肾上腺素耗竭，且右心室重量未恢复正常。所有未解除压力过载的压力过载心脏的心肌均表现出缩短速度降低和承受负荷能力降低。仅患有RVH的猫在压力解除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，但承受负荷的能力仍降低。我们得出结论，只要未发生充血性心力衰竭，压力过载损伤的心肌具有足够的恢复潜力。心力衰竭会导致心肌产生力量的能力持续降低。压力过载引起的心肌肥大，无论是否伴有CHF，都会导致心脏儿茶酚胺耗竭，这种耗竭不会因压力过载的解除而轻易逆转。
