Jacob R, Gülch R W, Ebrecht G
Med Klin. 1978 Mar 3;73(9):317-20.
An experimental study attempts to clarify the reasons for a fashionable over- or underestimation of the unloaded shortening velocity of the myocardium (Vmax) as an index of "contractility" in international cardiological literature. Long-term investigations on the isolated myocardial preparation as well as on the heart in situ support our own position: 1. Vmax of the myocardium is, without doubt, a value of greater relevance in muscle physiology independent of the interpretation related to the fundamental processes. 2. Vmax cannot be exclusively regarded as a function of the rate of cross-bridge movements, but is influenced by the Ca2+-concentration and consequently by the conditions of electromechanical coupling. 3. Vmax is not a reliable measure for myocardial power capacity under all conditions as this value on the one hand and the developed tension on the other are influenced to different degrees. 4. If the amount of contractile material per cross sectional unit is changed (changed relation of fibrils/mitochondria), Vmax can give better indications on the contractile elementary process than the developed tension. 5. Increased content of connective tissue and scars influence both the developed tension and Vmax. 6. A reduction in Vmax under long-term increased hemodynamic loading of the heart is not to be considered a priori as an expression of cellular damage.
一项实验研究试图阐明国际心脏病学文献中作为“收缩性”指标的心肌无负荷缩短速度(Vmax)为何会被时尚地高估或低估。对离体心肌标本以及原位心脏的长期研究支持了我们的观点:1. 心肌的Vmax在肌肉生理学中无疑是一个更具相关性的数值,与对基本过程的解释无关。2. Vmax不能仅仅被视为横桥运动速率的函数,而是受Ca2+浓度影响,进而受机电偶联条件影响。3. Vmax并非在所有情况下都是心肌功率容量的可靠指标,因为该值一方面与另一方面所产生的张力受到不同程度的影响。4. 如果每横截面积单位收缩物质的量发生变化(肌原纤维/线粒体关系改变),Vmax相较于所产生的张力能更好地反映收缩基本过程。5. 结缔组织和瘢痕含量增加会同时影响所产生的张力和Vmax。6. 长期心脏血流动力学负荷增加导致的Vmax降低,不应先验地被视为细胞损伤的表现。