Model dependent behaviour of pressure hypertrophied myocardium.
Model dependent behaviour of pressure hypertrophied myocardium.
复制标题
压力肥厚心肌的模型依赖性行为。
DOI：
10.1093/cvr/21.5.342
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发表时间：
1987
影响因子：
10.8
通讯作者：
Tomanek,RJ
中科院分区：
文献类型：
--
作者：
Cooper4th,G;Tomanek,RJ
使用对压力超负荷具有对比反应的两种动物模型来确定心功能障碍是压力肥厚心肌的一般特性还是特定模型的特定特性。比较了（a）成年和老年自发性高血压大鼠的左心室（其中压力超载从幼犬开始）和（b）成年猫的右心室（其中小猫通过手术开始压力超载）的慢性进行性心脏压力超负荷。对 9 只高血压大鼠和 9 只对照大鼠在 1 岁时进行了研究，此时高血压在该模型中处于稳定状态；然后对 2 岁时的五只高血压大鼠和五只对照大鼠进行了研究，此时两组大鼠都开始表现出明显的老年死亡率。两个高血压组的收缩压也同样升高。与血压正常对照组相比，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%。在左心室乳头肌等张收缩期间，各组对照组和高血压大鼠的肌肉缩短的程度和速度相同，但两个年龄组的高血压大鼠的肌肉的缩短和松弛时间均延长。在等长收缩过程中，产生了张力，并且张力上升的速率始终相同，但两个年龄组的高血压大鼠的肌肉中主动张力的时间积分均增加。高血压大鼠的肌肉中耗氧量与外部工作或产生的张力的比率降低。与这些数据相反，来自肥大猫模型的先前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减少，并且没有观察到收缩的延长。在肥厚的猫心肌中也发现了类似但较小的收缩需氧量下降。这些对比数据不仅表明压力引起的肥大在啮齿动物模型中具有更充分的代偿性，而且更重要的是，从任何特定动物肥大模型得出的一般结论可能是不合适的。
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.