Vogt M, Jacob R, Kissling G, Rupp H
Physiologisches Institut II, Universität Tübingen, F.R.G.
Basic Res Cardiol. 1987;82 Suppl 2:147-59. doi: 10.1007/978-3-662-11289-2_15.
Mechanical and energetic consequences of myocardial transformation and of ventricular configuration on the other were separately analysed. The considerations were realized on representative samples of normotensive rats and spontaneously hypertensive rats (SHR) in compensated stages, as well as in SHR in a state of congestive cardiac failure. Cardiac dynamic measurements were performed under Urethane anaesthesia and open chest conditions. Myosin isoenzyme pattern was determined by pyrophosphate gel electrophoresis. Energetic calculations were based on oxygen consumption data, measured in a specified heart-lung model. In the compensated stage of SHR the concentric type of left ventricular hypertrophy with renormalized systolic auxotonic wall stress predominated. The process of cardiac hypertrophy was associated with a shift in the myosin isoenzyme pattern towards the "slow" VM-3. Myocardial transformation did not significantly reduce myocardial performance and pumping ability, but caused a decrease in oxygen consumption as related to developed stress and LV weight. Thus, the efficiency of the hypertrophied ventricle of SHR was improved. However, due to the moderate effect of isoenzyme pattern redistribution for total energy turnover and the limited adaptive reserve of normotensive controls, the extent of improvement was small. In SHR with congestive heart failure, myocardial contractility was severely impaired, when structural dilatation of the left ventricle had set in. Reduced myocardial contractility could not be explained solely on the basis of a shift in the myosin isoenzyme pattern. Both impaired myocardial contractility and structural dilatation contributed to reduced ventricular performance. Myocardial transformation, along with its energy economizing effect, failed to compensate for unfavorable energetic consequences of structural dilatation and therefore the reduced ventricular efficiency is assumed to be another deleterious factor in the dilated failing heart.
分别分析了心肌转变和心室形态对彼此的机械和能量影响。研究对象为处于代偿期的正常血压大鼠和自发性高血压大鼠（SHR）的代表性样本，以及处于充血性心力衰竭状态的SHR。在氨基甲酸乙酯麻醉和开胸条件下进行心脏动力学测量。通过焦磷酸凝胶电泳确定肌球蛋白同工酶模式。能量计算基于在特定心肺模型中测量的耗氧量数据。在SHR的代偿期，以收缩期等张壁应力恢复正常的同心型左心室肥厚为主。心脏肥大过程伴随着肌球蛋白同工酶模式向“慢”VM-3的转变。心肌转变并未显著降低心肌性能和泵血能力，但与所产生的应力和左心室重量相关的耗氧量有所下降。因此，SHR肥厚心室的效率得到了提高。然而，由于同工酶模式重新分布对总能量代谢的影响适中，以及正常血压对照组的适应性储备有限，改善程度较小。在患有充血性心力衰竭的SHR中，当左心室出现结构扩张时，心肌收缩力严重受损。心肌收缩力降低不能仅基于肌球蛋白同工酶模式的转变来解释。心肌收缩力受损和结构扩张均导致心室性能下降。心肌转变及其能量节约效应未能补偿结构扩张带来的不利能量后果，因此心室效率降低被认为是扩张型衰竭心脏的另一个有害因素。
