Bohuslavs'kyĭ A Iu, Dmytriieva A V, Sahach V F
Fiziol Zh (1994). 2004;50(5):3-10.
On anaesthetized dogs the role of the mitochondrial permeability transition pore (mPTP) in the development of the m. gastrocnemius fatigue was investigated. In a control series of experiments it was shown, that 10 short-term (30") electrical stimulation (8 Hz, 5 ms, 20 V) with 5" interval resulted in significant reduction of the muscle contractions force (more than 40%) and considerably increased oxygen cost of a m. gastrocnemicus work (more than 130%), comparison with initial parameters. The registered inhibition of the muscle contraction force pointed on the development of m. gastrocnemius fatigue, that was accompanied by an appearance in blood from v. femoralis mitochondrial factor (MF), which, as shown by us earlier, is a marker of the mPTP opening. Preliminary injection of selective inhibitor of the mPTP opening cyclosporine A (0.012 mg/kg, i.v.) resulted in the pronounced fall of the MF concentration in blood from v. femoralis, in comparison with the parameters registered under control conditions. Pretreatment with the another inhibitor of the mPTP opening melatonin (0.75 mg/kg, i.v.) prevented inhibition of the muscle contractions force and reduction of the efficiency of oxygen using by m. gastercnemicus under conditions similar control. Thus, m. gastercnemius fatigue didn't develop, and the MF concentration in blood from v. femoralis was much lower, than in the control, that testified to absence of the mPTP opening. So then, fatigue development was accompanied by inhibition of the muscle contractions force, marked reduction of the efficiency of oxygen using by m.gastercnemicus that was prevented by the mPTP opening inhibitors. Thus, the mPTP opening can underlie the development of the working skeletal muscle fatigue.
在麻醉犬身上，研究了线粒体通透性转换孔（mPTP）在腓肠肌疲劳发展中的作用。在一系列对照实验中发现，10次短期（30秒）电刺激（8赫兹，5毫秒，20伏），间隔5秒，导致肌肉收缩力显著降低（超过40%），腓肠肌工作的氧耗显著增加（超过130%），与初始参数相比。记录到的肌肉收缩力抑制表明腓肠肌疲劳的发展，同时股静脉血中出现线粒体因子（MF），正如我们之前所示，这是mPTP开放的标志物。预先注射mPTP开放的选择性抑制剂环孢素A（0.012毫克/千克，静脉注射），与对照条件下记录的参数相比，导致股静脉血中MF浓度显著下降。用另一种mPTP开放抑制剂褪黑素（0.75毫克/千克，静脉注射）预处理，在类似对照的条件下，可防止肌肉收缩力的抑制和腓肠肌氧利用效率的降低。因此，腓肠肌疲劳未发展，股静脉血中MF浓度比对照低得多，这证明没有mPTP开放。所以，疲劳的发展伴随着肌肉收缩力的抑制、腓肠肌氧利用效率的显著降低，而mPTP开放抑制剂可防止这种情况。因此，mPTP开放可能是工作骨骼肌疲劳发展的基础。
