PURPOSE: To study the effects of anoxia and substrate depletion, both separately and combined, on the contractile responses of guinea-pig detrusor smooth muscle strips to activation of intrinsic nerves, application of agonists and depolarization with high potassium solution. MATERIALS AND METHODS: Bladders were opened and the urothelium removed. Strips of detrusor were dissected and mounted for tension recording in small organ baths superfused with warmed solutions of known composition. RESULTS: Anoxia caused a small initial reduction of the contractile responses which then remained constant for several hours. Glucose-free solutions resulted in a slow progressive decline in the responses to field stimulation, carbachol and high potassium solution, with substantial responses still present after five hours. The response to ATP, however, was unaffected. Removal of oxygen and glucose, mimicking ischaemia, caused abolition of all responses within an hour. After reintroduction of normal conditions responses reached their maximal extent of recovery within an hour. Recovery was almost complete for responses to ATP and carbachol, but less so for high K+ solutions. Very little recovery to stimulation of intrinsic nerves was seen. CONCLUSIONS: The results demonstrate that phasic contractions can be fuelled almost fully by oxidative phosphorylation or by anaerobic glycolysis, but that in conditions mimicking ischaemia the intrinsic nerves are more susceptible to ischaemic damage than the detrusor smooth muscle.
PURPOSE: To study the effects of anoxia and substrate depletion, both separately and combined, on the contractile responses of guinea-pig detrusor smooth muscle strips to activation of intrinsic nerves, application of agonists and depolarization with high potassium solution. MATERIALS AND METHODS: Bladders were opened and the urothelium removed. Strips of detrusor were dissected and mounted for tension recording in small organ baths superfused with warmed solutions of known composition. RESULTS:Anoxia caused a small initial reduction of the contractile responses which then remained constant for several hours. Glucose-free solutions resulted in a slow progressive decline in the responses to field stimulation, carbachol and high potassium solution, with substantial responses still present after five hours. The response to ATP, however, was unaffected. Removal of oxygen and glucose, mimicking ischaemia, caused abolition of all responses within an hour. After reintroduction of normal conditions responses reached their maximal extent of recovery within an hour. Recovery was almost complete for responses to ATP and carbachol, but less so for high K+ solutions. Very little recovery to stimulation of intrinsic nerves was seen. CONCLUSIONS: The results demonstrate that phasic contractions can be fuelled almost fully by oxidative phosphorylation or by anaerobic glycolysis, but that in conditions mimicking ischaemia the intrinsic nerves are more susceptible to ischaemic damage than the detrusor smooth muscle.