1 School of Public Health, State University of New York at Albany , Rensselaer, New York.
2 National Center for Adaptive Neurotechnologies, Wadsworth Center , New York State Department of Health, Albany, New York.
J Neurotrauma. 2017 Nov 1;34(21):3012-3026. doi: 10.1089/neu.2016.4844. Epub 2017 Jun 30.
The rat is a commonly used model for the study of lower urinary tract function before and after spinal cord injury. We have previously reported that in unanesthetized freely moving rats, although phasic external urethral sphincter (EUS) activity (bursting) is most common during micturition, productive voiding can occur in the absence of bursting, which differs from results seen in anesthetized or unanesthetized restrained animals. The purpose of the present study was to characterize EUS behavior in unanesthetized, freely moving rats before and after mid-thoracic (T8) or thoraco-lumbar (T13-L1) spinal transection to determine how EUS behavior after spinal cord injury differs from that seen in anesthetized or unanesthetized restrained rats. Several abnormalities became evident that were comparable after transection at either level, including the following: repetitive non-voiding EUS contractions; increased prevalence, intensity, and duration of EUS bursting; decreased rate of urine evacuation during bursting; increased void size and decreased number of daily voids; shorter inter-burst silent period and increased frequency of bursting; and loss of the direct linear relationships that are evident in intact animals between void size and bursting silent period. These data suggest that transection-induced delayed initiation of EUS bursting allows co-contraction of the bladder and the EUS that prevents or limits urine evacuation, resulting in a detrusor-sphincter dyssynergia-like phenomenon. In addition, the higher-than-normal frequency at which EUS bursting occurs after transection is associated with shorter silent periods during which urine typically flows, which interferes with voiding by slowing the rate of urine evacuation. That results were comparable after either transection suggests that the central pattern generator responsible for EUS bursting is located caudal to the L1 spinal segment.
大鼠是研究脊髓损伤前后下尿路功能的常用模型。我们之前曾报道过，在未麻醉的自由活动大鼠中，尽管排尿时外尿道括约肌（EUS）的相位活动（爆发）最为常见，但在没有爆发的情况下也可以进行有产尿，这与麻醉或未麻醉的束缚动物的结果不同。本研究的目的是描述 T8 或 T13-L1 脊髓横切前后未麻醉、自由活动大鼠的 EUS 行为，以确定脊髓损伤后 EUS 行为与麻醉或未麻醉束缚大鼠的行为有何不同。在 T8 或 T13-L1 脊髓横切后，出现了一些明显的异常，包括以下几点：重复的非排尿性 EUS 收缩；EUS 爆发的发生率、强度和持续时间增加；爆发期间尿液排空率降低；尿排量增加，每日排尿次数减少；EUS 爆发的间歇期缩短，爆发频率增加；以及在完整动物中明显的尿排量和 EUS 爆发间歇期之间的直接线性关系丧失。这些数据表明，横切诱导的 EUS 爆发延迟启动允许膀胱和 EUS 的共同收缩，从而阻止或限制尿液排空，导致逼尿肌-括约肌协同失调样现象。此外，横切后 EUS 爆发的频率高于正常，与通常尿液流动的间歇期缩短有关，这通过降低尿液排空率来干扰排尿。两种横切后结果相似表明，负责 EUS 爆发的中枢模式发生器位于 L1 脊髓节段以下。
