Urethra is more sensitive to ischemia than bladder: Evidence from an in vitro rat study
Urethra is more sensitive to ischemia than bladder: Evidence from an in vitro rat study
复制标题
DOI：
10.1016/s0022-5347(05)66299-4
复制
发表时间：
2001-06-01
影响因子：
6.6
通讯作者：
Levin, RM
中科院分区：
文献类型：
--
作者：
Bratslavsky, G;Kogan, B;Levin, RM
目的：实验研究表明，缺血可导致严重的膀胱功能障碍。由于导致膀胱缺血的多种原因也会减少尿道灌注，因此我们评估了体外缺血对大鼠膀胱和尿道收缩反应的影响。我们评估了尿道缺血性损伤中神经源性功能障碍发生在肌源性功能障碍之前的假设。我们还比较了大鼠膀胱和尿道的收缩反应，在体外缺血，然后通过reoxygenation.Materials和方法：大鼠膀胱逼尿肌和前列腺尿道分离条孵育在正常的生理介质和电和化学刺激。通过将组织在缺血培养基中孵育30或60分钟来产生体外缺血。数字化分析缺血前和缺血后再灌注后的最大张力和最大张力产生率。仅在尿道中并且仅响应于场刺激而产生的张力的速率显著降低。在缺血60分钟后，尿道收缩反应的减少大于膀胱收缩反应的减少。缺血60分钟的持续时间造成了显着下降的最大速率产生的张力，以及最大张力在尿道和膀胱，但只有在响应领域stimulation.Conclusions：本实验表明，尿道是更敏感的缺血性损伤比膀胱。我们的发现可以解释在膀胱功能障碍出现之前，括约肌损伤继发的尿失禁的发展和症状。我们还表明，在膀胱和尿道的反应场（神经源性）刺激是最敏感的形式的刺激缺血。
Purpose: Experimental studies have demonstrated that ischemia may induce significant bladder dysfunction. Because multiple causes leading to bladder ischemia also decrease urethral perfusion, we assessed the effect of in vitro ischemia on the contractile responses of the rat bladder and urethra. We evaluated the hypothesis that neurogenic dysfunction in urethral ischemic injury occurs before myogenic dysfunction is present. We also compared contractile responses of the rat bladder and urethra to in vitro ischemia followed by reoxygenation.Materials and Methods: Isolated strips of rat bladder detrusor muscle and prostatic urethra were incubated in normal physiological medium and stimulated electrically and chemically. In vitro ischemia was produced by incubating tissue in ischemic medium for 30 or 60 minutes. The maximal tension and maximal rate of tension generated were analyzed digitally before ischemia and after ischemia followed by reoxygenation.Results: We demonstrated that after 30 minutes of ischemia followed by reperfusion the maximal. rate of tension generated decreased significantly only in the urethra and only in response to field stimulation. After 60 minutes of ischemia the decrease in urethral contractile responses was greater than the decrease in bladder contractile responses. Ischemia 60 minutes in duration caused a significant decrease in the maximal rate of tension generated as well as maximal tension in the urethra and bladder but only in response to field stimulation.Conclusions: This experiment demonstrates that the urethra is more sensitive to ischemic injury than the bladder. Our finding may explain the development and symptoms of urinary incontinence secondary to sphincteric damage before bladder dysfunction is present. We also demonstrated that in the bladder and urethra the response to field (neurogenic) stimulation is the most sensitive form of stimulation to ischemia.