Effect of respiratory acidosis and activity on airway smooth muscle intracellular pH

Abstract

Respiratory acidosis (RA) impaired mechanical function in canine tracheal smooth muscle (TSM). Since an intracellular acidosis was brought on by the increased CO2 content of the bathing medium and altered the Km of rate-limiting glycolytic enzymes in the pathway of energy production for contractile function, the effects of RA on the intracellular pH (pHi) of TSM was investigated. Using the DMO [dimethadione] method, paired unstimulated or resting TSM strips were incubated under normocapnic conditions (P[partial pressure]O2 600 Torr, PCO2 40 Torr, pH 7.40) and RA (P O2 550 Torr, PCO2 110 Torr, pH 6.95) with 14C-labeled DMO and 3H-inulin or PEG[polyethylene glycol]-4000. In another set of paired experiments, TSM strips were tetanized electrically every 5 min or pharmacologically throughout the incubation period (active muscle strips). The tissue and an aliquot of bathing medium were counted for 3H and 14C content and the values entered into the Waddell and Butler equation. The pHi of resting normocapnic and acidotic strips were 7.041 .+-. 0.017 (SE) and 6.752 .+-. 0.012, respectively. However, the pHi of active normocapnic and acidotic strips were 7.275 .+-. 0.017 and 7.017 .+-. 0.015, respectively. RA lowered pHi in both resting and mechanically active TSM; however, active preparations whether exposed to normocapnia or acidosis were unexpectedly more alkaline than their resting counterparts.