Cooper G, Tomanek R J
Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania.
Cardiovasc Res. 1987 May;21(5):342-51. doi: 10.1093/cvr/21.5.342.
Two animal models with contrasting responses to pressure overloading were used to determine whether cardiac dysfunction is a general property of pressure hypertrophied myocardium or a specific property of a particular model. Chronic progressive cardiac pressure overload was compared in (a) the left ventricle of the adult and aged spontaneously hypertensive rat, in which pressure overloading begins in the pup, and (b) the right ventricle of the adult cat, in which pressure overloading was initiated surgically in the kitten. Nine hypertensive and nine control rats were studied at 1 year of age, when hypertension is stable in this model; five hypertensive and five control rats were then studied at 2 years of age, when both groups of rats are beginning to show appreciable senile mortality. Systolic blood pressure was similarly increased in both hypertensive groups; compared with the normotensive control groups, the ratio of left ventricular to body weight was 36% and 76% higher in the 1 and 2 year old hypertensive groups respectively. During isotonic contractions of left ventricular papillary muscles the extent and velocity of shortening in muscles from the control and hypertensive rats in each group were the same, but shortening and relaxation times were prolonged in muscles from the hypertensive rats in both age groups. During isometric contractions developed tension and the rate of tension rise were the same throughout, but the time integral of active tension was increased in muscles from the hypertensive rats in both age groups. The ratio of oxygen consumption to either external work or developed tension was decreased in muscles from the hypertensive rats. In contrast to these data, previous data from the hypertrophied cat model showed reductions in both the velocity and the extent of isotonic shortening as well as in the rate and amount of isometric tension development, and prolongation of contraction was not observed. A similar but smaller decrease in the oxygen requirements of contraction was found in hypertrophied cat myocardium. These contrasting data suggest not only that pressure induced hypertrophy is more fully compensatory in the rodent model but, more importantly, that general conclusions derived from any particular animal model of hypertrophy may be inappropriate.
使用两种对压力超负荷反应截然不同的动物模型，以确定心脏功能障碍是压力性肥厚心肌的普遍特性还是特定模型的特殊特性。在以下两种模型中比较慢性进行性心脏压力超负荷情况：(a) 成年和老年自发性高血压大鼠的左心室，其压力超负荷始于幼崽期；(b) 成年猫的右心室，其压力超负荷是在小猫期通过手术引发的。对9只高血压大鼠和9只对照大鼠在1岁时进行研究，此时该模型中的高血压已稳定；然后对5只高血压大鼠和5只对照大鼠在2岁时进行研究，此时两组大鼠都开始出现明显的老年死亡率。两个高血压组的收缩压均同样升高；与正常血压对照组相比，1岁和2岁高血压组的左心室与体重之比分别高出36%和76%。在左心室乳头肌的等张收缩过程中，每组对照大鼠和高血压大鼠肌肉的缩短程度和速度相同，但两个年龄组高血压大鼠肌肉的缩短和舒张时间均延长。在等长收缩过程中，整个过程中的发展张力和张力上升速率相同，但两个年龄组高血压大鼠肌肉的主动张力时间积分增加。高血压大鼠肌肉的氧耗量与外部功或发展张力之比降低。与这些数据形成对比的是，之前来自肥厚猫模型的数据显示，等张缩短的速度和程度以及等长张力发展的速率和量均降低，且未观察到收缩延长。在肥厚猫心肌中发现收缩氧需求有类似但较小的降低。这些截然不同的数据不仅表明压力诱导的肥厚在啮齿动物模型中更具完全代偿性，更重要的是，从任何特定的肥厚动物模型得出的一般结论可能并不恰当。
