慢性吸煙經由增加氧化壓力和細胞凋亡，減少 nNOS、內皮和平滑肌含量而損害大鼠勃起功能
黃雲慶、陳志碩、林威宇、何東儒、林健輝、黃國財
財團法人嘉義長庚紀念醫院 外科部 泌尿科
Chronic cigarette smoking impairs erectile function through increased oxidative stress and apoptosis, decreased nNOS, endothelial and smooth muscle contents in a rat model
Yun-Ching Huang, Chih-Shou Chen, Wei-Yu Lin, Dong-Ru Ho, Jian-Hui Lin, Guo-Cai Huang
Division of Urology, Department of Surgery, Chang Gung Memorial Hospital, Chiayi, Taiwan
Purpose: Cigarette use is an independent risk factor for the development of erectile dysfunction (ED). While the association between chronic smoking and ED is well established, the fundamental mechanism(s) of cigarette-related ED are incompletely understood, partly due to no reliable animal model of smoking-induced ED. The present study was designed to validate an in vivo rat model of chronic cigarette-induced ED.
Materials and Methods: Forty 12-week old male Sprague-Dawley rats were divided into 4 groups. Ten rats served as control group and were exposed only to room air. The remaining 30 rats were passively exposed to cigarette smoke (CS) for 4 weeks (n=10), 12 weeks (n=10), and 24 weeks (n=10). At the 24-week time point all rats were assessed with intracavernous pressure (ICP) during cavernous nerve electrostimulation. Blood and urine were collected to measure serum testosterone and oxidative stress, respectively. Corporal tissue was assessed by Western blot for neuronal nitric oxide synthase (nNOS). Penile tissues were subjected to immunohistochemistry for endothelial, smooth muscle, and apoptotic content.
Results: Mean arterial pressure (MAP) was significantly higher in 24-week cigarette exposed animals compared to the control animals. Mean ICP/MAP ratio and cavernosal smooth muscle/endothelial contents were significantly lower in the 12- and 24-week rats compared to control animals. Oxidative stress was significantly higher in the 24-week cigarette exposed group compared to control animals. Mean nNOS expression was significantly lower, and apoptotic index significantly higher, in CS-exposed animals compared to control animals.
Conclusion: These findings indicate that the rat model exposure to CS increases apoptosis and oxidative stress and decreases nNOS, endothelial and smooth muscle contents, and ICP in a dose dependent fashion. The rat model is a useful tool for further study of the molecular and cellular mechanisms of CS-related ED.