Dekalo Snir, Stern Noah, Broderick Gregory A, Brock Gerald
Division of Urology, Western University, Department of Surgery, London, ON, Canada.
Division of Urology, Western University, Department of Surgery, London, ON, Canada.
Sex Med Rev. 2022 Oct;10(4):660-668. doi: 10.1016/j.sxmr.2022.06.007. Epub 2022 Aug 24.
Ischemic priapism remains a significant cause of morbidity among men. To date, the precise time when penile ischemia results in permanent, non-reversible cavernosal smooth muscle injury, compromising subsequent erectile integrity, remains ill-defined.
To review the medical literature pertaining to ischemic priapism, focusing on factors that predict the exact timeline of irreversible cavernous tissue injury.
A comprehensive literature search was performed. Our search included both publications on animal models and retrospective clinical series through January 2022. Articles were eligible for inclusion if they contained original data regarding nonreversible tissue injury on histology and/or provided a timeline of erectile function loss or preservation and had full text available in English.
Innovative studies in the 1990s using invitro models with strips of rabbit, rat, canine and monkey corpus cavernosal tissue demonstrated that anoxia eliminated spontaneous contractile activity and reduced tissue responsiveness to electrical field stimulation or pharmacological agents. The same models demonstrated that the inhibitory effects of field stimulated relaxation, were mediated by nitric oxide. Subsequent studies using similar models demonstrated that exposure of corpus cavernosum smooth muscle to an acidotic environment impairs its ability to contract. A pH of 6.9 was chosen for these experiments based on a case series of men with priapism, in whom a mean pH of 6.9 was measured in corporal blood after 4-6 hours of priapism. Invivo animal studies demonstrated that after erection periods of 6-8 hours, microscopy shows sporadic endothelial defects but otherwise normal cavernous smooth muscle. In these studies, greater durations of ischemic priapism were shown to result in more pronounced ultrastructural changes and presumably irreversibility. In studies involving human corporal tissues, samples were obtained from men who had experienced priapism for at least 12 hours. Overall, erectile function outcome data is deficient in priapism reporting, especially within treatment windows less than 6 hours. Some reports on ischemic priapism have documented good erectile function outcomes with reversal by 12 hours.
Based on our extensive review of animal models and clinical reports, we found that many clinical papers rely on the same small set of animal studies to suggest the time point of irreversible ischemic damage at 4-6 hours. Our review suggests an equal number of retrospective clinical studies demonstrate that ischemic priapism reversed within 6-12 hours may preserve erectile function in many patients. Dekalo S, Stern N, Broderick GA, et al. Priapism or Prolonged Erection: Is 4 - 6 Hours of Cavernous Ischemia the Time Point of Irreversible Tissue Injury? Sex Med Rev 2022;10:660-668.
缺血性阴茎异常勃起仍然是男性发病的一个重要原因。迄今为止，阴茎缺血导致海绵体平滑肌永久性、不可逆损伤，进而损害后续勃起功能的具体时间仍不明确。
回顾与缺血性阴茎异常勃起相关的医学文献，重点关注预测海绵体组织不可逆损伤确切时间线的因素。
进行了全面的文献检索。我们的检索包括截至2022年1月关于动物模型的出版物和回顾性临床系列研究。如果文章包含关于组织学上不可逆组织损伤的原始数据和/或提供了勃起功能丧失或保留的时间线，并且有英文全文，则符合纳入标准。
20世纪90年代使用兔、大鼠、犬和猴海绵体组织条带的体外模型进行的创新性研究表明，缺氧消除了自发收缩活动，并降低了组织对电场刺激或药物的反应性。相同的模型表明，电场刺激舒张的抑制作用是由一氧化氮介导的。随后使用类似模型的研究表明，海绵体平滑肌暴露于酸中毒环境会损害其收缩能力。基于一系列阴茎异常勃起男性的病例，这些实验选择了6.9的pH值，在阴茎异常勃起4 - 6小时后，海绵体内血液的平均pH值为6.9。体内动物研究表明，勃起6 - 8小时后，显微镜检查显示散在的内皮缺陷，但海绵体平滑肌其他方面正常。在这些研究中，缺血性阴茎异常勃起持续时间越长，超微结构变化越明显，可能越不可逆。在涉及人体海绵体组织的研究中，样本取自经历阴茎异常勃起至少12小时的男性。总体而言，阴茎异常勃起报告中勃起功能结果数据不足，尤其是在治疗窗口小于6小时的情况下。一些关于缺血性阴茎异常勃起的报告记录了在12小时内恢复后良好的勃起功能结果。
基于我们对动物模型和临床报告的广泛回顾，我们发现许多临床论文依赖于同一小部分动物研究来表明4 - 6小时是不可逆缺血损伤时间点。我们的回顾表明，同样数量的回顾性临床研究表明，在6 - 12小时内恢复的缺血性阴茎异常勃起在许多患者中可能保留勃起功能。德卡洛S、斯特恩N、布罗德里克GA等。阴茎异常勃起或持续性勃起：6 - 12小时的海绵体缺血是不可逆组织损伤的时间点吗？性医学评论2022；10：660 - 668。
