RECUPERATION DE LA CONTRACTILITE MYOCARDIQUE DURANT L'ACIDOSE HYPERCAPNIQUE: SA DIASSOCIATION DE LA RECUPERATION A UN PHI PAR LA RYANODINE

Myocardial contractility falls quickly during respiratory acidosis but if acidosis is maintained a slow gradual return towards control state is detected. In cat papillary muscle, changes in developed tension (DT) during isometric contractions (pacing rate 0.2 Hz) and intracellular pH (pH(i)) were continuously monitored before and during hypercapnia to study the contribution of pH(i) recovery to the recovery of contractility. On exposure to hypercapnia (extracellular pH [pH(o)]=6.90) DT fell to 50.33±2.20% of control and pH(i) decreased from 7.21±0.05 to 6.90±0.02. After 30 mins of hypercapnia DT recovered to 64.66±4.05% of control, but no significant recovery in pH(i) was detected. Intracellular sodium concentration slowly rose to 61.05±23.79% over basal level 10 mins after the onset of hypercapnia and it remained elevated for 10 mins before gradually returning to control levels. When pH(o) was kept at 7.40 during hypercapnia by increasing sodium bicarbonate concentration, DT recovered to 79.11±6.94% of control after 30 mins of hypercapnia, while a significant recovery of pH(i) (0.12±0.02 pH units) was detected. Low extracellular sodium concentration diminished contractility recovery during hypercapnia without changing the initial decrease in DT. 5-[N-ethyl-N-iso-propyl] amiloride (EIPA) (5μM) increased the initial fall in DT to 34.33±8.68% of control and abolished the recovery. Sarcoplasmic reticulum (SR) inhibition by ryanodine (0.5μM) markedly reduced the recovery of contractility without altering the recovery in pH(i). The authors conclude that the magnitude of myocardial contractility recovery during hypercapnia acidosis is related to the extent of Na⁺/H⁺ exchange activation and requires a functional SR to be expressed fully.