Myocardial oxygen consumption: the role of wall force and shortening.
Myocardial oxygen consumption: the role of wall force and shortening.
复制标题
心肌耗氧量：室壁力和缩短的作用。
DOI：
10.1152/ajpheart.1977.233.4.h421
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发表时间：
1977
期刊：
影响因子：
--
通讯作者：
J. S. Janicki
中科院分区：
文献类型：
--
作者：
K. Weber;J. S. Janicki
测定收缩期左室壁力与心肌耗氧量（MVO2）的关系。此外，还评估了缩短和纤维缩短过程中施加的载荷对MVO2的相对影响。为此，我们使用了14个伺服调节的、有节奏的、离体的犬心脏，并测量了冠状动脉总流量和动静脉氧差的稳态反应。对于等容跳动和射室，MVO2与收缩力积分之间存在统计学上显著的线性关系。这些关系彼此之间没有显著差异，表明缩短不是MVO2的决定因素。此外，在等效发展力的等距喷射时，发现了MVO2 （deltaMVO2）的差异。deltaMVO2是这些收缩之间的力积分差的函数，而不是纤维缩短的函数。因此，在本实验条件下，在任何给定的收缩状态下，收缩力（包括展开力和缩短载荷）的积分是调节MVO2的主要因素，而纤维缩短的影响可以忽略不计。
The relationship between the force in the left ventricular wall during systole and myocardial O2 consumption (MVO2) was determined. In addition, the relative influence of the load imposed during shortening and fiber shortening on MVO2 was assessed. For this purpose, 14 servo-regulated, paced, isolated canine hearts were used and the steady-state response in total coronary flow and arteriovenous oxygen difference was measured. For both the isovolumetrically beating and the ejecting ventricle, statistically significant linear relations were observed between MVO2 and the integral of systolic force. These relations were not significantly different from one another, indicating that shortening was not a determinant of MVO2. Moreover, when ejecting an isolumetric beats of equivalent developed force were compared, a difference in MVO2 (deltaMVO2) was found. deltaMVO2 was a function of the force integral difference between these contractions and not fiber shortening. Thus, under the conditions of this experiment, the integral of systolic force that includes developed force and shortening load is the predominant factor regulating MVO2 for any given contractile state, whereas the influence of fiber shortening is negligible.