Bettice J A, Owens D, Riley S
Respir Physiol. 1984 Jan;55(1):121-30. doi: 10.1016/0034-5687(84)90121-x.
The intracellular pH (pHi) and bicarbonate concentration ([HCO3-]icw) of cardiac and skeletal muscles were monitored during respiratory alkalosis in order to further elucidate the homeostatic processes which operate in these tissues to ameliorate deviations from normal acid-base status. Rats were mechanically hyperventilated to induce hypocapnia, pHi was determined by the DMO method, and [HCO-3]icw was calculated from the Henderson-Hasselbalch equation using pHi and the partial pressure of carbon dioxide of vena caval blood. A significant intracellular alkalosis occurred in both cardiac and skeletal muscles during hypocapnia, but the changes in pHi were less in the heart than in skeletal muscle. The decreases in cardiac [HCO-3]icw were greater than those attributable to the physicochemical buffering of the heart. These data are consistent with an intramyocardial source of protons other than physicochemical buffering during respiratory alkalosis. The decreases in skeletal muscle [HCO-3]icw were less than those due to physicochemical buffering. These data are consistent with a net extrusion from skeletal muscles cells of the protons derived from physicochemical buffering during respiratory alkalosis.
在呼吸性碱中毒期间监测心脏和骨骼肌的细胞内pH值（pHi）和碳酸氢盐浓度（[HCO3-]icw），以进一步阐明这些组织中维持稳态的过程，这些过程可改善与正常酸碱状态的偏差。对大鼠进行机械过度通气以诱导低碳酸血症，通过DMO法测定pHi，并使用pHi和腔静脉血二氧化碳分压根据Henderson-Hasselbalch方程计算[HCO-3]icw。低碳酸血症期间，心脏和骨骼肌均出现明显的细胞内碱中毒，但心脏中pHi的变化小于骨骼肌。心脏中[HCO-3]icw的降低幅度大于心脏物理化学缓冲作用所致的降低幅度。这些数据与呼吸性碱中毒期间除物理化学缓冲作用外心肌内质子的来源一致。骨骼肌中[HCO-3]icw的降低幅度小于物理化学缓冲作用所致的降低幅度。这些数据与呼吸性碱中毒期间骨骼肌细胞对物理化学缓冲产生的质子进行净排出一致。
