PH CONTROL IN RAT SKELETAL-MUSCLE DURING EXERCISE, RECOVERY FROM EXERCISE, AND ACUTE RESPIRATORY-ACIDOSIS
PH CONTROL IN RAT SKELETAL-MUSCLE DURING EXERCISE, RECOVERY FROM EXERCISE, AND ACUTE RESPIRATORY-ACIDOSIS
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DOI：
10.1002/mrm.1910310203
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发表时间：
1994-02-01
影响因子：
3.3
通讯作者：
RADDA, GK
中科院分区：
文献类型：
--
作者：
KEMP, GJ;THOMPSON, CH;RADDA, GK
我们使用P-31磁共振波谱比较大鼠骨骼肌对三种质子负荷的反应。在运动期间（强直性坐骨神经刺激），乳酸的质子被被动缓冲，并被磷酸肌酸（PCr）的净水解消耗。在运动恢复期间，阿米洛利或4，4 '-二异硫氰基芪-2，2'-二磺酸盐（DIDS）可部分抑制PCr再合成产生的质子的pH依赖性流出，涉及钠/质子和碳酸氢盐/氯离子交换，但不受同时呼吸性酸中毒的抑制。在早期恢复，高达30%的质子流出是由乳酸/质子共转运介导的。在急性呼吸性酸中毒在休息时，肌肉pH值的最终变化是一致的被动缓冲，并不受阿米洛利或DIDS，这意味着质子通量没有显着的贡献。
We used P-31 magnetic resonance spectroscopy to compare the response of rat skeletal muscle to three kinds of proton load. During exercise (tetanic sciatic nerve stimulation), protons from lactic acid were buffered passively and consumed by net hydrolysis of phosphocreatine (PCr). During recovery from exercise, the pH-dependent efflux of protons produced by PCr resynthesis could be partially inhibited by amiloride or 4,4'diisothiocyanostilbene-2,2'-disulphonate (DIDS), implicating both sodium/proton and bicarbonate/chloride exchange, but was not inhibited by simultaneous respiratory acidosis. In early recovery, up to 30% of proton efflux was mediated by lactate/proton cotransport. During acute respiratory acidosis at rest, the eventual change in muscle pH was consistent with passive buffering and was unaffected by amiloride or DIDS, implying no significant contribution of proton fluxes.