RESUMO
PURPOSE: Previous studies concerning the ischemic priapism revealed that hypoxia alter the erectile and contractile responses of penis. But the effects of accompaning acidosis on the trabecular smooth muscle contractility have not been fully evaluated or understood yet. We performed this study to elucidate the role of acidosis on the trabecular smooth muscle contractility like in ischemic priapism. MATERIALS AND METHODS: Under the general anesthesia, 55 mature male cats were conditioned to systemic metabolic acidosis by hypoventilation with animal ventilator. The changes of intracavernous pressure to erectics(acetylcholine, L-arginine, PGE1), erectolytics(epinephrine, TXA2), K+-channel-related drugs (pinacidil, 4-aminopyridine, TEA, glibenclamide) and calcium ionophore were monitored at Set 1 (PO2>60mmHg, pH>7.25), Set 2(PO2 pH>7.0), Set 3(PO260mmHg, pH<7.0) in vivo. RESULTS: At Set 1 and Set 2, the acetylcholine or PGE1-induced relaxations were suppressed by epinephrine, TXA2 or ionomycin(n=9, p<0.01). The contractility was in order of epinephrine, TXA2 and ionomycin. Cavernous relaxations to acetylcholine or PGE1 were reduced by acidosis(n=8, p<0.01). TXA2 or ionomycin did not produced contraction even with higher concentration but epinephrine maintained contractility with higher concentration at acidosis (n=7, p<0.05). Acidosis-induced relaxation was not prevented by 4-aminopyridine, TEA, or glibenclamide(n=6, p<0.05). Pinacidil did not induced relaxation at acidosis(n=6, p<0.01). CONCLUSIONS: Acidosis impairs the contractile response of cavernous smooth muscle to submaximal stimulation with erectolytics. It may be the results of the interference by(H+) with the intra and extracellular mechanisms that regulate the homeostasis of(Ca2+). Conclusively, acidosis is another limiting factor of trabecular smooth muscle contractility like in ischemic priapism.