Nerve injury‐related erectile dysfunction following nerve‐sparing radical prostatectomy: A novel experimental dissection model

Abstract

Objectives: To establish a new experimental rat model in order to define the mechanisms of erectile dysfunction (ED) and to evaluate the changes of neuronal nitric oxide synthase (nNOS) in the pelvic ganglia following nerve‐sparing radical prostatectomy. Methods: Sprague‐Dawley rats were randomized to sham operation, bilateral cavernous nerve dissection (BCND) and bilateral cavernous nerve resection (BCNR) groups. In the BCND group, the cavernous nerves were only dissected bilaterally from the major pelvic ganglion (MPG) to the apex of the prostate without crushing or cutting. At 1, 2, 4 and 8 weeks after surgery, we examined intracavernous pressure along with arterial pressure (ICP/AP), retrograde dye tracing using Fluorogold (FG) and expression of nNOS in the MPG. Results: Intracavernous pressure and arterial pressure in the BCND group was significantly decreased at 2 and 4 weeks after surgery compared with the sham group, and improved at 8 weeks. The number of FG‐positive cells in the MPG also recovered at 8 weeks. ICP/AP and FG‐positive cells in the BCNR group were greatly decreased until 8 weeks. The percentage of nNOS‐positive cells per total cells was not different between the sham and BCND groups during the experimental period, whereas that in the BCNR group gradually decreased with time. Conclusions: We established a novel rat model, in which cavernous nerve dissection alone caused nerve injury‐related ED. We believe that this cavernous nerve dissection model might help clarify the mechanism of nerve injury‐related ED and the recovery from ED after nerve‐sparing radical prostatectomy.