Background: The aim of this project was to develop an ex-vivo porcine bladder model to test the effects of increasing durations of acute ischemia on detrusor function.
Methods: Porcine bladders were perfused through bilateral vesical arteries at physiologic flow (4 mL/min) and filled through a urethral catheter. Intravesical pressures were continuously recorded using standard urodynamics equipment. Bladder contractions, with simulated voiding, were induced by arterial infusion of KCl at 250 mL. Total, passive, and active pressures were recorded for each contraction and data were normalized to the control fill. Bladders underwent the following perfusion protocol by adjusting the arterial flow rates: Equilibration (4 mL/min), control (4 mL/min), partial ischemia (2 mL/min), global ischemia (0 mL/min) and reperfusion (4 mL/min). Perfusion periods were held for 15 min for one group and 30 min for another group of bladders.
Results: Porcine bladders (N=19) including 8 (15 min group) and 11 (30 min group) were used. With 15 min ischemia, passive pressure increased 39% (P=0.03) and the active pressure decreased 23% (P=0.002). Total pressure remained constant, identifying a compensated phase. Values returned to baseline with reperfusion. With 30 min ischemia, passive pressure remained unchanged. However, there was a decrease in total pressure 34% (P<0.001) and active pressure 61% (P<0.001), which incompletely recovered to baseline values, identifying a decompensated phase with incomplete recovery upon reperfusion.
Conclusion: In the porcine bladder, 15 min ischemia resulted in a compensated phase and 30 min ischemia resulted in a decompensated phase of detrusor function. This study provides mechanistic insight into the natural history of ischemia-mediated voiding dysfunction.
Keywords: Animal model; bladder; ischemia; muscle contraction.
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