目的 建立一种神经性勃起功能障碍（ED）大鼠模型，对其进行评价并探讨该模型可能的发病机制。 方法 将 SD 大鼠随机分为假手术组和神经性 ED 组，神经性 ED 组大鼠通过双侧海绵体神经挤压法进行手术 造模。术后 3 周后通过交配实验和海绵体内压（ICP）测量实验评估大鼠勃起功能；通过 Masson 染色观察大鼠海 绵体纤维化水平、离体肌张力（Tension）实验检测大鼠海绵体平滑肌舒张功能；通过免疫荧光法测定海绵体组 织一氧化氮（NO）释放情况以及酶联免疫吸附法测定海绵体组织环磷酸鸟苷（cGMP）含量，探究该模型可能的发 病机制。结果 与假手术组比较，神经性 ED 组大鼠捕捉次数与插入次数减少（P＜0.05）、插入潜伏期延长 （P＜0.05），海绵体内压下降（P＜0.001），海绵体组织纤维化水平上升（P＜0.05），苯肾上腺素（PE）引发海绵体 平滑肌收缩增加（P＜0.05），而电场刺激（EFS）引起的海绵体平滑肌舒张减少（P＜0.01，P＜0.001），海绵体组 织内 NO 及 cGMP 表达量减少（P＜0.01，P＜0.001）。结论 该研究通过双侧海绵体神经挤压法成功建立了神经 性 ED 大鼠模型，发病机制可能与 NO-cGMP 通路下调有关，可为进一步的中药药效评价研究以及药理机制探 讨等提供可靠的动物模型。

Objective To establish a rat model of neurogenic erectile dysfunction （ED） and evaluate it comprehensively，while exploring the potential pathogenesis of the model. Methods SD rats were randomly divided into a sham-operated group and a neurogenic ED group. The neurogenic ED group underwent bilateral cavernous nerve crush surgery to establish the model. Three weeks post-surgery，the rats’ erectile function was assessed using mating behavior tests and intracavernous pressure （ICP） measurements. Masson staining was used to evaluate the level of fibrosis in the corpus cavernosum， and in vitro tension experiments were conducted to assess the relaxation function of cavernous smooth muscle. Immunofluorescence was used to measure nitric oxide （NO） release in the corpus cavernosum，and enzyme-linked immunosorbent assay （ELISA） was used to determine the cyclic guanosine monophosphate （cGMP） content in the corpus cavernosum，aiming to explore the potential pathogenesis of the model. Results Compared with the sham-operated group， the neurogenic ED group showed a significant reduction in the number of captures and intromissions （P＜0.05）， prolonged intromission latency （P＜0.05）， decreased intracavernous pressure （P＜0.001），increased fibrosis in the corpus cavernosum （P＜0.05），enhanced phenylephrine （PE）-induced contraction of cavernous smooth muscle （P＜0.05）， and reduced electrical field stimulation （EFS）-induced relaxation of cavernous smooth muscle （P＜0.01，P＜0.001）. Additionally，the expression levels of NO and cGMP in the corpus cavernosum were significantly reduced （P＜0.01，P＜0.001）. Conclusion This study successfully established a rat model of neurogenic ED using bilateral cavernous nerve crush surgery. The pathogenesis may be related to the downregulation of the NO-cGMP pathway. This model provides a reliable animal model for further research on the efficacy evaluation of traditional Chinese medicine and the exploration of pharmacological mechanisms.

R285.5

国家自然科学基金项目（82074107）；广东省教育厅重点领域专项（2021ZDZX2018）