The development of rat models induced by cavernous nerve injury
Yan-Ping Huang1, Mu-Jun Lu2, Jonathan Clavell-Hernandez3, Run Wang3
1 Department of Urology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Andrology, Shanghai, China; Division of Urology, Department of Surgery, University of Texas Medical School at Houston; Department of Urology, University of Texas MD Anderson Cancer Center, Houston, TX, USA
2 Department of Urology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Andrology, Shanghai, China
3 Division of Urology, Department of Surgery, University of Texas Medical School at Houston; Department of Urology, University of Texas MD Anderson Cancer Center, Houston, TX, USA
Department of Urology, University of Texas Mcgovern Medical School and MD Anderson Cancer Center, 6431 Fannin Street, MSB 6.018 Houston, Texas 77030
Source of Support: None, Conflict of Interest: None
Background and Objective: Erectile dysfunction (ED) caused by iatrogenic cavernous nerve injury (CNI) is a common complication in males undergoing pelvic surgery. Despite the advances in surgical techniques and the regular administration of phosphodiesterase type 5 inhibitors (PDE5i), recovery from CNI-induced ED remains to be a difficult process. Numerous CNI models have been established to explore the pathogenesis and design effective therapies suitable for human trials. This study aims to examine the studies referring to rat models of CNI induced ED. Methods: A literature review was performed through PubMed using the items “CNI” and “rat model.” We analyzed different types of CNI, the pathophysiology changes after CNI, and current and future strategies of therapy after CNI. Results: A large number of rat models with CNI-induced ED have been established for mimicking ED pathophysiology after radical pelvic surgery. The types of injury include crush, transection, excision, dissection, freezing, electrocautery, and irradiation. The pathophysiological assessments include changes in hemodynamics, nerve structure and morphology, oxidative stress, and inflammation of genes in the corpus cavernosum. The current therapeutic strategies include PDE5i administration, vacuum erection device, and other treatments aiming to decrease known pathologic damages. The future treatment direction may focus on gene transfer, growth factors (nerve and endothelium), cellular scaffolds, and endogenous stem cells to the penis. Conclusions: The CNI rat models are important experimental methods to mimic the nerve damage caused by the treatment of prostate cancer. Many research studies have demonstrated significant pathophysiological changes that occur in rat cavernous bodies after CNI. The ideal model for CNI-induced ED should be explored furthermore to improve the slow recovery of erectile function following CNI.