Gonzalez N C, Wemken H G, Heisler N
Respir Physiol. 1981 Oct;46(1):1-6. doi: 10.1016/0034-5687(81)90063-3.
Intracellular pH (pHi) of triceps, trapezius, quadriceps and gastrocnemius muscle tissue was determined in rats with myocardial hypertrophy due to experimental aortic stenosis (AS) and in sham operated rats (SO). During normocapnia, no significant difference in pHi between AS and So animals was observed in any of the muscle species investigated. In hypercapnia (FICO2 0.06, 0.075 or 0.100) pHi of AS was significantly higher than pHi of SO in all muscles, despite no difference in pHe, PaCO2 or [HCO3]a between AS and SO. Therefore, AS appears to be associated with an improvement of pHi regulation in skeletal muscle. In this respect, skeletal muscle behaves as hypertrophic cardiac muscle, which also shows an increased ability to regulate pHi in AS. These results suggest that the changes in pHi regulation of hypertrophic myocardium are not due to the hypertrophic process per se, but to a general phenomenon secondary to AS.
在因实验性主动脉狭窄（AS）导致心肌肥大的大鼠以及假手术大鼠（SO）中，测定了肱三头肌、斜方肌、股四头肌和腓肠肌组织的细胞内pH值（pHi）。在正常碳酸血症期间，在所研究的任何肌肉种类中，未观察到AS大鼠和SO大鼠之间pHi有显著差异。在高碳酸血症（FICO2为0.06、0.075或0.100）时，尽管AS大鼠和SO大鼠之间的细胞外pH值（pHe）、动脉血二氧化碳分压（PaCO2）或动脉血碳酸氢根浓度（[HCO3]a）无差异，但所有肌肉中AS大鼠的pHi均显著高于SO大鼠。因此，AS似乎与骨骼肌中pHi调节的改善有关。在这方面，骨骼肌的表现与肥厚性心肌相似，后者在AS中也显示出调节pHi的能力增强。这些结果表明，肥厚性心肌中pHi调节的变化并非由于肥厚过程本身，而是由于AS继发的一种普遍现象。
