Graham T E, Barclay J K, Wilson B A
J Appl Physiol (1985). 1986 Feb;60(2):568-75. doi: 10.1152/jappl.1986.60.2.568.
The effects of respiratory acidosis on glycolysis in the autoperfused canine gastrocnemius-plantaris were studied using anesthetized dogs that were ventilated either with air (n = 30) or with 4% CO2-21% O2-75% N2 (n = 30). The left muscle group was stimulated at 3 Hz for up to 20 min, after which the active and the contralateral resting muscles were removed and frozen in liquid N2. Blood flow, VO2, Vco2, and tension development were unaffected by CO2. Glycogen catabolism was not affected, but lactate release (La) was lower (P less than 0.05) during activity with CO2; and greater fructose 6-phosphate, fructose 6-phosphate/fructose 1,6-diphosphate, and alpha-glycerophosphate/dihydroxyacetone phosphate ratios resulted (P less than 0.05). With respiratory acidosis, muscle lactate tended to accumulate early in contractions, but a net lactate uptake occurred during the last 10 min of contractions. Thus, respiratory acidosis reduced lactate efflux and there was a net uptake late in the contraction period. Glycogen phosphorylase did not appear to be affected by the respiratory acidosis, but there was evidence of inhibition at the phosphofructokinase step as well as a tendency for lactate to accumulate within the muscle. La often occurred in a direction contrary to the muscle-venous lactate concentration difference with either air or CO2 and La also decreased far more rapidly over time than did the arterial-venous H+.
利用麻醉犬研究了呼吸性酸中毒对自灌注犬腓肠肌 - 比目鱼肌糖酵解的影响，这些犬分别用空气（n = 30）或4%二氧化碳 - 21%氧气 - 75%氮气（n = 30）进行通气。左侧肌肉群以3赫兹频率刺激长达20分钟，之后将活动的肌肉和对侧静息肌肉切除并在液氮中冷冻。血流、耗氧量、二氧化碳排出量和张力发展不受二氧化碳影响。糖原分解代谢未受影响，但在二氧化碳通气期间活动时乳酸释放（La）较低（P < 0.05）；并且果糖6 - 磷酸、果糖6 - 磷酸/果糖1,6 - 二磷酸和α - 甘油磷酸/二羟基丙酮磷酸的比值升高（P < 0.05）。发生呼吸性酸中毒时，肌肉乳酸在收缩早期趋于积累，但在收缩的最后10分钟出现净乳酸摄取。因此，呼吸性酸中毒减少了乳酸外流，并且在收缩期后期有净摄取。糖原磷酸化酶似乎不受呼吸性酸中毒影响，但有证据表明在磷酸果糖激酶步骤受到抑制，并且肌肉内有乳酸积累的趋势。无论是空气通气还是二氧化碳通气，乳酸往往朝着与肌肉 - 静脉乳酸浓度差相反的方向出现，并且乳酸随时间下降的速度也比动脉 - 静脉氢离子下降的速度快得多。
