Tracey Andrew T, Anele Uzoma A, Vince Randy A, Speich John E, Klausner Adam P, Ratz Paul H
Division of Urology, Department of Surgery, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Department of Mechanical and Nuclear Engineering, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Transl Androl Urol. 2019 Dec;8(6):703-711. doi: 10.21037/tau.2019.11.12.
The deleterious effects of chronic ischemia on bladder function have been extensively studied; however, evaluation and characterization of the effects of acute ischemia and hypoxia are lacking. The present study examined pig and human detrusor smooth muscle (DSM) strips, in combination with an isolated perfused working pig bladder model to evaluate the relationship between transient ischemia and bladder function.
Organ bath and myographic studies were performed using pig and human DSM strips exposed to starvation/hypoxia conditions. Analogous conditions were then recreated in the ex vivo bladder preparation. Filled bladders were then treated with intravascular carbachol to induce contraction and subsequent void. An intravesical transducer continuously monitored changes in bladder pressure, while a tissue pO monitor analyzed changes in oxygenation.
After 120 min in starved/hypoxic conditions, both pig and human DSM strips demonstrated significantly increased resting tone, with a greater than two-fold increase in force over control. This was effectively blocked with atropine. DSM strips also demonstrated significantly weaker contractions; however, contractile force was nearly recovered following 15-min exposure to replete/oxygenated buffer. In the ex vivo bladder preparation, filling under ischemic conditions yielded a 225% increase in end-fill vesical pressures (P) compared to controls. End-fill P returned to baseline with reperfusion during a subsequent filling cycle.
Transient ischemia/hypoxia leads to an acute increase in tone in both DSM strips and ex vivo pig bladder. Remarkably, the effect is reversible with re-perfusion and may be blocked with anticholinergics, suggesting a relationship between acute ischemia and increased local acetylcholine release.
慢性缺血对膀胱功能的有害影响已得到广泛研究；然而，急性缺血和缺氧影响的评估与特征描述尚显不足。本研究检测了猪和人的逼尿肌平滑肌（DSM）条带，并结合孤立灌注的工作猪膀胱模型，以评估短暂缺血与膀胱功能之间的关系。
使用暴露于饥饿/缺氧条件下的猪和人DSM条带进行器官浴和肌动描记研究。然后在离体膀胱制备中重现类似条件。随后用血管内卡巴胆碱处理充盈的膀胱以诱导收缩和随后的排尿。膀胱内换能器持续监测膀胱压力变化，而组织pO监测仪分析氧合变化。
在饥饿/缺氧条件下120分钟后，猪和人的DSM条带均显示静息张力显著增加，力量比对照组增加两倍以上。这被阿托品有效阻断。DSM条带还显示收缩明显减弱；然而，在暴露于充足/充氧缓冲液15分钟后，收缩力几乎恢复。在离体膀胱制备中，与对照组相比，缺血条件下充盈使终末充盈膀胱压力（P）增加225%。在随后的充盈周期中，再灌注时终末充盈P恢复到基线。
短暂缺血/缺氧导致DSM条带和离体猪膀胱的张力急性增加。值得注意的是，这种效应在再灌注后是可逆的，并且可能被抗胆碱能药物阻断，提示急性缺血与局部乙酰胆碱释放增加之间存在关联。
