Structural and functional changes associated with failure and recovery of hearts after perfusion with Ca2+-free medium.
Structural and functional changes associated with failure and recovery of hearts after perfusion with Ca2+-free medium.
复制标题
灌注无 Ca2 培养基后与心脏衰竭和恢复相关的结构和功能变化。
DOI：
10.1016/0022-2828(75)90011-5
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发表时间：
1975
影响因子：
5
通讯作者：
N. Dhalla
中科院分区：
文献类型：
--
作者：
John C. Yates;N. Dhalla
本实验观察了离体大鼠心脏在无钙灌流和无钙灌流不同时间后再灌注正常心肌时的电、机械功能和超微结构。收缩力下降到零内灌注与Ca 2+的培养基。无钙灌注3分钟内未观察到超微结构变化;然而，无钙灌注5分钟或更长时间后以及无钙灌注3分钟后用正常培养基再灌注时，注意到闰盘分离。正常介质再灌注后心脏恢复收缩力的能力取决于无钙灌注的持续时间。静息张力在无钙灌注期间增加，并在2 min后用正常培养基再灌注时进一步增加。无钙灌注5 min或更长时间后用正常培养基再灌注也导致肌节挛缩和广泛的超微结构损伤。不可逆的变化，表面电活动发生后3至4分钟的无钙灌注。降低Na+浓度的无钙介质延迟收缩性的失败，增强收缩性的恢复，并防止分离的闰盘。降低Mg 2+浓度的Ca 2 +-无培养基也延迟收缩性失败，但不影响恢复。降低K+浓度并不能改变衰竭的时间进程，但会减少无Ca 2+灌注3分钟后收缩力的恢复。这些结果阐明了Ca 2+剥夺过程中发生的结构和功能变化的顺序，并支持细胞外Na+在Ca 2+剥夺心脏衰竭过程中起有害作用的观点。这表明，离体心脏灌流与Ca ~（2+）-free培养基形成了一个有趣的模型，用于研究两种类型的心力衰竭，即失败，由于“细胞内钙缺乏”和失败，由于“细胞内钙超载”的发病机制。
The electrical and mechanical functions and ultrastructure of isolated rat hearts were studied during perfusion with Ca2+-free medium and during reperfusion with normal medium following various intervals of Ca2+-free perfusion. Contractile force declined to zero within 30 s of perfusion with Ca2+-free medium. No ultrastructural changes were observed within 3 min of Ca2+-free perfusion; however, separation of the intercalated discs was noted after 5 min or longer of Ca2+-free perfusion and upon reperfusion with normal medium after 3 min of Ca2+-free perfusion. The ability of hearts to recover contractile force upon reperfusion with normal medium was dependent upon the duration of the Ca2+-free perfusion. The resting tension was increased during the Ca2+-free perfusion and was further increased upon reperfusion with normal medium after 2 min. Reperfusion with normal medium after 5 min or longer of Ca2+-free perfusion also resulted in contracture of sarcomeres and extensive ultrastructural damage. Irreversible changes in surface electrical activity occurred after 3 to 4 min of Ca2+-free perfusion. Reducing the Na+concentration of the Ca2+-free medium delayed failure of contractility, augmented the recovery of contractility, and prevented the separation of the intercalated discs. Reducing the Mg2+concentration of the Ca2+-free medium also delayed failure of contractility but did not affect recovery. Reducing the K+concentration did not alter the time-course of failure but diminished the recovery of contractile force after 3 min of Ca2+-free perfusion. These results clarify the sequence of structural and functional changes occurring during Ca2+deprivation and support the view that extracellular Na+plays a deleterious role during failure of Ca2+-deprived hearts. It is suggested that isolated heart perfused with Ca2+-free medium forms an interesting model for studying the pathogenesis of two types of heart failure namely failure due to “intracellular calcium deficiency” and failure due to “intracellular calcium overload”.