Neurourology and Urodynamics 25:388^396 (2006) External Urethral Sphincter Activity in a Rat Model of Pudendal Nerve Injury Chih-Wei Peng, 1 Jia-Jin Jason Chen, 1 Hui-Yi Chang, 1,2 William C. de Groat, 2 and Chen-Li Cheng 3 * 1 Institute of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan, Republic of China 2 Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 3 Division of Urology, Department of Surgery,Taichung Veterans General Hospital,Taichung,Taiwan, Republic of China Aims: Pudendal nerve injury in the rat has been a useful animal model for studying stress urinary incontinence (SUI). However, the e¡ect of pudendal nerve injury on activity of the external urethral sphincter (EUS) is relatively unexplored. The aims of this study were to examine voiding and the EUS electromyogram (EMG) in a durable SUI model in rats with bilateral or unilateral pudendal nerve transections. In addition, the e¡ects of denervation on urethral anatomy were investigated. Methods: A leak point pressure (LPP) test was ¢rst used to demonstrate that pudendal nerve trans- ection induced SUI. Cystometry exhibited changes in voiding function and EUS-EMG measure- ments provided a quantitative evaluation of EUS activity during voiding. The morphological changes in sections through the mid-urethra were assessed with hematoxylin and eosin (H&E) staining. Results: A signi¢cant decrease in average LPP was detected in rats 6 weeks after bilateral pudendal nerve transection (BPNT). Abnormal urodynamic measurements including a decrease in contraction amplitude and voided volume as well as an increase in contraction duration, and resi- dual volume all indicated ine⁄cient voiding. In addition EUS-EMG silent periods were reduced and the frequency of EUS-EMG bursting during voiding was increased. Atrophy of striated muscle in the EUS was also detected in rats with pudendal nerve transection(s). Conclusions: Our results indicate that pudendal nerve transection in rats decreases urethral outlet resistance and causes striated muscle atrophy in the EUS, EUS-EMG abnormalities and ine⁄cient voiding. The results demonstrate that BPNT is a durable model for SUI. Neurourol. Urodynam. 25:388 ^396, 2006. ß 2006 Wiley-Liss, Inc. Key words: cystometrographic; electromyogram; leak point pressure; stress urinary incon- tinence; voiding INTRODUCTION Stress urinary incontinence (SUI) is one of the most com- mon forms of incontinence among middle aged women [Thom and Brown, 1998]. It can be de¢ned as involuntary loss of urine through the urethra secondary to a sudden increase of abdominal pressure in the absence of detrusor contraction during events such as sneezing, coughing or laughing. A demographic survey indicated that SUI occurs in 37.7% of noninstitutionalized women older than 60 years of age and in 33.9% of women over 40 years of age. SUI is associated with a decrease in urethral resistance [Kayigil et al., 1999] that results from general diseases, surgical trauma, and childbirth. Child- birth by vaginal delivery is considered to be a dominant epide- miological factor, leading to injury of the pudendal nerves, pelvic £oor muscles and connective tissues that maintain con- tinence [Damaser et al., 2003]. Avariety of animal models have been proposed to elucidate the possible mechanisms of SUI [Kerns et al., 2000; Sakamoto et al., 2000; Sievert et al., 2001; Cannon et al., 2002; Damaser et al., 2003; Chermansky et al., 2004; Rodriguez et al., 2005]. Pudendal nerve injury [Kerns et al., 2000; Sakamoto et al., 2000; Damaser et al., 2003] has been one of the most common models used to simulate SUI. However, previous studies [Kerns et al., 2000; Sakamoto et al., 2000] indicated that crush- ing the pudendal nerves in the female rat only induced mild urinary incontinence. Furthermore, urinary continence gra- dually recovered 2 weeks following the injury when evalua- tions were performed. Most investigations of SUI in rats measured voiding beha- vior, voided volume (VV), urinary frequency, leak point No con£ict of interest reported by the author(s). This paper was received, reviewed, and accepted by the previous editorial board under the leadership of the past editor, Dr. Jerry Blaivas. Grant sponsor: Industrial Technology Research Institute; Grant numbers: NSC93-2213-E-075A-002, NSC94-2314-B-075A-019; Grant sponsor: National Science Council,Taiwan. *Correspondence to: Dr. Chen-Li Cheng, Division of Urology, Department of Surgery, Taichung Veterans General Hospital, Taichung 407, Taiwan, Republic of China. E-mail: cheng20011@yahoo.com.tw Received 8 August 2005; Accepted 2 January 2006 Published online 24 April 2006 inWiley InterScience (www.interscience.wiley.com) DOI 10.1002/nau.20229 ß 2006Wiley-Liss,Inc.