Waste of ATP for tension development in myocardial acidosis: chemomechanical uncoupling at myofibrillar level.
Waste of ATP for tension development in myocardial acidosis: chemomechanical uncoupling at myofibrillar level.
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心肌酸中毒张力发展中 ATP 的浪费：肌原纤维水平的化学机械解偶联。
DOI：
10.1016/0022-2828(90)91109-k
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发表时间：
1990
影响因子：
5
通讯作者：
S. Hosoda
中科院分区：
文献类型：
--
作者：
T. Takayasu;T. Toyo;S. Hosoda
心肌缺血发生后早期收缩衰竭的确切机制仍不清楚。生理学研究报道，细胞内无机磷酸盐积累和细胞内酸中毒是收缩衰竭的主要因素[3,9,10]。相反，生化实验表明，随着培养pH值的降低，肌原纤维ATP酶的Ca2+敏感性降低，但最大肌原纤维ATP酶活性没有变化[1, 11]。
The precise mechanism responsible for the early contractile failure after the onset of myocardial ischemia remains unclear. Physiological studies have reported that intracellular accumulation of inorganic phosphate and intracellular acidosis are the main factors of contractile failure [3, 9, 10]. In contrast, biochemical experiments have shown that the Ca2+sensitivity of myofibrillar ATPase became less as incubation pH reduces, but the maximal myofibrillar ATPase activity did not change [1, 11].
心脏收缩蛋白的调节。
影响因子：
20.1
作者：
Winegrad,S
通讯作者：
Winegrad,S