Adaptive and pathological alterations in experimental cardiac hypertrophy.
Adaptive and pathological alterations in experimental cardiac hypertrophy.
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实验性心脏肥大的适应性和病理性改变。
DOI：
10.1007/978-1-4757-4441-5_4
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
H. Rupp
中科院分区：
文献类型：
--
作者：
R. Jacob;G. Kissling;G. Ebrecht;C. Holubarsch;I. Medugorac;H. Rupp
基于对各种实验性心脏肥大模型（肾性高血压、自发性高血压、主动脉瓣狭窄、游泳训练、甲状腺毒症）的研究，人们试图描述肥厚过程所固有或伴随的适应性和病理性改变。原则上，将过程指定为适应性的植根于目的论的观点，并且意味着相应的结构和功能改变的基本趋势适合于应对改变的功能需求。然而，这并不意味着这种改变在所有条件下和所有肥大阶段都是有利的。由于生物体通常表现出相对刻板的反应模式，因此“适应性”和“病理性”这两个术语归根结底并不相互排斥。在长期压力负荷的心室中，几乎所有变化都是不明确的（心肌质量增加、动作电位延长、细胞内收缩物质过度增加、肌原纤维 ATP 酶活性降低）。 ATPase 活性的改变是基于肌球蛋白同工酶模式向同工酶 V3 方向的转变，伴随着无负荷缩短速度的降低，但张力发展效率的提高，这反映在等容条件下整个心脏的耗氧量（单位壁应力和心率）减少。基本收缩过程和肌原纤维 ATP 酶活性的这种变化不必先验地解释为负面的。然而，适应其他类型负荷的能力，例如伴随心率相应增加的体力消耗，受到应对增强压力负荷的专门化的限制。 “过度适应”一词应保留用于肥大的阶段和程度，其中双面改变的负面影响占主导地位。压力负荷的快速过度增加以及长期的血流动力学超负荷会导致心肌的退行性改变。在整个心室水平，结构扩张导致心脏效率降低。心室壁纤维化的发病机制并不总是明确的，也是机械性能的负面因素。由于存在显着程度的肥大而没有结缔组织增加，例如在甲状腺毒症中，纤维化和伴随的心肌扩张性降低显然不一定与肥大的发展有关。血管病变引起的缺血引起的改变应与肥大引起的变化区分开来。游泳训练大鼠心脏的适应性改变涉及肌原纤维 ATP 酶活性的增加和肌球蛋白同工酶模式向 V1 方向的转变，导致各个水平的功能能力增加，这与普遍接受的收缩性概念一致。
Based on investigations of various models of experimental cardiac hypertrophy (renal hypertension, spontaneous hypertension, aortic stenosis, swimming training, thyrotoxicosis), an attempt has been made to characterize adaptive and pathological alterations that are inherent to or accompany the process of hypertrophy. In principle, the designation of a process as adaptive is rooted in a teleological point of view and implies that the basic tendency of the respective structural and functional alterations is appropriate for coping with the altered functional requirements. This does not mean, however, that such alterations are favorable under all conditions and in all stages of hypertrophy. Since organisms generally reveal relatively stereotypic reaction patterns, the terms “adaptive” and “pathological” are not mutually exclusive in the final analysis. In the chronically pressure-loaded ventricle, nearly all alterations are ambiguous (myocardial mass increase, prolongation of the action potential, overproportional increase of intracellular contractile material, decrease of myofibrillar ATPase activity). The altered ATPase activity, which is based on a shift in the isoenzyme pattern of myosin in the direction of isoenzyme V3, is accompanied by a decrease in unloaded shortening velocity but an increase in the efficiency of tension development, as is reflected in reduced oxygen consumption (per wall stress and heart rate) of the whole heart under isovolumetric conditions. This change in the elementary contractile process and the myofibrillar ATPase activity need not be interpreted a priori as negative. However, the ability to adapt to other types of loading, e.g., physical exertion with corresponding increase in heart rate, is limited by the specialization for coping with enhanced pressure load. The term “overadaptation” should be reserved for stages and degrees of hypertrophy in which the negative effects of double-faced alterations predominate. Rapid, excessive increase in pressure loading, as well as long-term hemodynamic overloading, leads to degenerative alterations of the myocardium. At the level of the whole ventricle, structural dilatation results in a decreased cardiac efficiency. Fibrosis of the ventricular wall, the pathogenesis of which is not always unequivocal, is also a negative factor for mechanical performance. Since there are pronounced degrees of hypertrophy without connective tissue increase, e.g., in thyrotoxicosis, fibrosis and accompanying decreased distensibility of the myocardium apparently are not necessarily involved in the development of hypertrophy. Ischemically induced alterations stemming from vasculopathy should be distinguished from hypertrophy-induced changes. The adaptive alteration of the heart in swim-trained rats, which involves an increase in myofibrillar ATPase activity and a shift in the myosin isoenzyme pattern in the direction of V1, leads to an increase in functional capacity at all levels and is in agreement with the generally accepted concept of contractility.