Coronary perfusion and muscle lengthening increase cardiac contraction: different stretch-triggered mechanisms
Coronary perfusion and muscle lengthening increase cardiac contraction: different stretch-triggered mechanisms
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DOI：
10.1152/ajpheart.00113.2002
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发表时间：
2002-10-01
影响因子：
4.8
通讯作者：
Westerhof, N
中科院分区：
文献类型：
--
作者：
Lamberts, RR;Van Rijen, MHP;Westerhof, N
冠状动脉灌注增加，心肌横向拉伸，通过激活拉伸激活离子通道（SAC）增加了发展力（F-dev）（Gregg效应）。肌肉的拉长、心肌的纵向拉伸导致Fdev立即增加，随后F-dev缓慢增加（Anrep效应）。在等距收缩灌注的Wistar大鼠乳头肌中，我们通过测量F-dev和细胞内Ca 2+浓度来研究这两种效应是否基于相似的牵张诱导机制（[Ca 2 +]（i））在肌肉长度从85%增加到95% L-max后（最大等长力发展时的长度）在低和高冠状动脉灌注前和后用钆（10 mumol/l Gd 3+）抑制SAC。Gregg效应引起的F-dev和峰值[Ca 2 +]（i）的增加幅度与Anrep效应相似（从3.5 +/- 0.8至3.9 +/- 1.2 mN/mm（2）和从3.0 +/- 0.7%至3.8 +/- 0.9%标准化[Ca 2 +]（i），平均值+/- SE）。SAC阻断完全减弱了Gregg效应引起的Fdev和峰值[Ca 2 +]（i）的增加;然而，它不影响Anrep效应。缓慢的力反应，但不是钙反应，增加冠状动脉灌注。因此，增加冠状动脉灌注，心肌的横向拉伸，以及肌肉延长，心肌的纵向拉伸，通过不同的拉伸触发机制增加大鼠心肌收缩。
An increase in coronary perfusion, transversal stretch of the myocardium, increases developed force (F-dev) (Gregg effect) through activation of stretch-activated ion channels (SACs). Lengthening of the muscle, longitudinal stretch of the myocardium, causes an immediate increase in Fdev followed by a slow F-dev increase (Anrep effect). In isometrically contracting perfused papillary muscles of Wistar rats, we investigated whether both effects were based on similar stretch-induced mechanisms by measuring F-dev and intracellular Ca2+ concentration ([Ca2+](i)) after a muscle length increase from 85% to 95% L-max (length at which maximal isometric force develops) at low and high coronary perfusion before and after inhibition of SACs with gadolinium (10 mumol/l Gd3+). The increase of F-dev and peak [Ca2+](i) by the Gregg effect was of similar magnitude as the Anrep effect (from 3.5 +/- 0.8 to 3.9 +/- 1.2 mN/mm(2) and from 3.0 +/- 0.7% to 3.8 +/- 0.9% normalized [Ca2+](i), means +/- SE). SAC blockade completely blunted the increase of Fdev and peak [Ca2+](i) by the Gregg effect; however, it did not affect the Anrep effect. The slow force response, but not the calcium response, was augmented by an increase in coronary perfusion. Therefore, increased coronary perfusion, transversal stretch of the myocardium, and muscle lengthening, longitudinal stretch of the myocardium, increase myocardial contraction in the rat through different stretch-triggered mechanisms.