Stephens N L, Kroeger E A, Loh W
Am J Physiol. 1977 Mar;232(3):E330-5. doi: 10.1152/ajpendo.1977.232.3.E330.
Hypoxia impairs contractility in canine tracheal smooth muscle (TSM). This is attributed to intracellular lactacidosis. The present studies were undertaken to confirm this. Lactate was found to be significantly increased in hypoxic TSM (65.36 +/- 7.37 mg/100 g wet tissue), compared to normoxic (29.83 +/- 5.05). Intracellular pH (pHi) was, however, significantly increased in hypoxic active TSM to 7.71 +/- 0.05 as compared to 7.30 +/- 0.03 in normoxic active muscle. pHi of resting normoxic muscle (7.20 +/- 0.04) was statistically not different from that of resting hypoxic muscle. The pHi's of resting normoxic and active hypoxic muscles were significantly different. These results show that under in vitro, hypoxic conditions: 1) an increase in glycolysis in TSM is indicated by the increased lactate production, 2) there is a surprising, concomitant rise in pHi rather than a decrease as previously expected, and 3) it is mechanical activity of the muscle which leads to this paradoxical result, inasmuch as pHi is unaltered in the resting hypoxic muscle.
缺氧会损害犬气管平滑肌（TSM）的收缩能力。这归因于细胞内乳酸酸中毒。进行本研究以证实这一点。与常氧状态（29.83±5.05）相比，缺氧TSM中的乳酸显著增加（65.36±7.37mg/100g湿组织）。然而，与常氧活性肌肉中的7.30±0.03相比，缺氧活性TSM中的细胞内pH（pHi）显著升高至7.71±0.05。静息常氧肌肉的pHi（7.20±0.04）与静息缺氧肌肉的pHi在统计学上无差异。静息常氧肌肉和活性缺氧肌肉的pHi有显著差异。这些结果表明，在体外缺氧条件下：1）TSM中糖酵解增加表现为乳酸生成增加；2）pHi出现令人惊讶的同时升高，而不是如先前预期的降低；3）是肌肉的机械活动导致了这一矛盾结果，因为静息缺氧肌肉中的pHi未改变。
