Kemp G J, Thompson C H, Sanderson A L, Radda G K
MRC Biochemical and Clinical Magnetic Resonance Unit, John Radcliffe Hospital, Oxford, United Kingdom.
Magn Reson Med. 1994 Feb;31(2):103-9. doi: 10.1002/mrm.1910310203.
We used 31P 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.
我们使用31P磁共振波谱来比较大鼠骨骼肌对三种质子负荷的反应。在运动期间（强直坐骨神经刺激），来自乳酸的质子被被动缓冲，并通过磷酸肌酸（PCr）的净水解而消耗。在运动恢复期间，PCr再合成产生的质子的pH依赖性外流可被氨氯吡脒或4,4'-二异硫氰基芪-2,2'-二磺酸盐（DIDS）部分抑制，这涉及钠/质子和碳酸氢根/氯离子交换，但不受同时存在的呼吸性酸中毒的抑制。在早期恢复过程中，高达30%的质子外流由乳酸/质子协同转运介导。在静息时的急性呼吸性酸中毒期间，肌肉pH的最终变化与被动缓冲一致，且不受氨氯吡脒或DIDS的影响，这意味着质子通量没有显著贡献。
