Adenosine output from dog gracilis muscle during systemic hypercapnia and/or amiloride-SITS infusion

Abstract

The influence of acidosis on adenosine output from the isolated constant- flow-perfused gracilis muscle was studied in anesthetized dogs. Depression of intracellular pH (pH(i)) by supplementation of the inspired air with 10% CO2-90% O2 increased arterial PCO2 from 34.2 ± 1.0 to 53.5 ± 1.9 mmHg, arterial PO2 from 138.3 ± 3.9 to 256.6 ± 17.6 mmHg, and venoarterial adenosine concentration from 14 ± 15 to 47 ± 19 nM. Twitch contractions of the muscle at 2 Hz increased venoarterial adenosine concentration to 165 ± 63 and 204 ± 62 nM in normocapnia and hypercapnia, respectively. Venoarterial lactate concentration increased from 0.42 ± 0.07 to 0.90 ± 0.15 mM during normocapnic contractions but remained unchanged during hypercapnic contractions (0.42 ± 0.11 mM). Depression of pH(i) by infusion of amiloride and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid increased venoarterial adenosine concentration from -2 ± 27 to 124 ± 48 nM in normocapnia and from 16 ± 24 to 236 ± 119 nM in hypercapnia. These results indicate that adenosine output from red oxidative skeletal muscle was stimulated by procedures that depress pH(i).