THE SPONTANEOUSLY HYPERTENSIVE RAT AS A MODEL OF THE TRANSITION FROM COMPENSATED LEFT-VENTRICULAR HYPERTROPHY TO FAILURE
THE SPONTANEOUSLY HYPERTENSIVE RAT AS A MODEL OF THE TRANSITION FROM COMPENSATED LEFT-VENTRICULAR HYPERTROPHY TO FAILURE
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DOI：
10.1016/s0022-2828(08)80035-1
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发表时间：
1995-01-01
影响因子：
5
通讯作者：
CONRAD, CH
中科院分区：
文献类型：
--
作者：
BING, OHL;BROOKS, WW;CONRAD, CH
通过血流动力学和左心室心肌功能的研究，探讨衰老（18-24个月）自发性高血压大鼠（SHR）从稳定肥厚到心脏失代偿的转变过程。清醒动物的超声心动图数据显示，与年龄匹配的高血压（SHR- np）和非高血压对照动物（WKY）相比，SHR衰竭（SHR- f）左心室舒张末期和收缩末期容积增加，射血分数降低。麻醉动物的心导管数据显示收缩压和+dP/dt均下降，相对于两个对照组，SHR-F的舒张末期压升高。由于负荷条件和需求状态的改变可能导致心室功能的改变，对分离的灌注心脏进行的研究表明，在负荷条件得到控制的情况下，SHR-F组的收缩应激发育受损；此外，我们观察到灌注压力增加30 mmHg对功能的影响很小。收缩功能的降低和SHR-F分离肌肉制剂被动僵硬度的增加表明在组织水平上收缩和舒张功能受损。虽然所有研究的制剂都有潜在的缺点，但综合这些互补方法的研究结果支持心力衰竭在衰老的SHR中发生的结论。此外，这些数据表明，功能受损是由于心肌固有特性的改变，结缔组织反应可能起重要作用。这些研究与其他研究SHR衰老的研究结果相结合，为使用衰老SHR作为代偿性肥大向衰竭过渡的模型提供了支持。
Studies of hemodynamics and intrinsic left ventricular myocardial function are carried out to investigate the transition from stable hypertrophy to cardiac decompensation in the aging (18-24 months) spontaneously hypertensive rat (SHR). Echocardiographic data in awake animals demonstrate increased end-diastolic and end-systolic volumes and depressed ejection fractions in left ventricles from SHR with failure (SHR-F) as compared to age matched hypertensive (SHR-NP) and non-hypertensive control animals (WKY). Cardiac catheterization data in anesthetized animals demonstrate depression of both systolic pressure and +dP/dt, and elevated end-diastolic pressure in the SHR-F relative to the two control groups, Since loading conditions and altered demand states may contribute to altered ventricular function, studies of isolated perfused hearts were carried out which demonstrate impaired systolic stress development in the SHR-F group under conditions in which loading conditions are controlled; in addition, it is observed that increasing perfusion pressure by 30 mmHg has little effect on function. Depression of systolic function and increases in passive stiffness of isolated muscle preparations from the SHR-F indicate impairment of systolic and diastolic function at the tissue level. While all of the preparations studied have potential shortcomings, an integration of findings from these complementary approaches supports the conclusion that heart failure develops in the aging SHR. Furthermore, these data suggest that impaired function is due to changes in the intrinsic properties of the myocardium and that the connective tissue response may play an important role, These studies, in conjunction with the findings of others who have studied the aging SHR, provide support for the use of the aging SHR as a model of the transition from compensated hypertrophy to failure.