We developed a rat model of traumatic arteriogenic erectile dysfunction (ED) for the study of vasculogenic ED. Bilateral ligation of the internal iliac artery was performed on 30 three-month old male Sprague-Dawley rats as an experimental group. The control group consisted of 12 rats which underwent dissection of the internal iliac artery without ligation. Before their euthanization at 3 days, 7 days, and 1 month (10 rats in the experimental group and four rats in the control group at each time point), erectile function was assessed by electrostimulation of the cavernous nerves. Penile tissues were collected for nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase staining, trichrome staining, electron microscopy and RT-PCR for transforming growth factor beta (TGF-beta1), insulin like growth factor-I (IGF-I) and fibroblast growth factors (FGF) mRNA expression. Electrostimulation of the cavernous nerves revealed a highly significant declining of the intracavernous pressure after 3 and 7 days. No significant recovery of erectile function was noted at 1 month. Histology showed degeneration of the dorsal nerve fibers in all experimental rats. There was little decrease in the bulk of intracavernous smooth muscle in the experimental rats euthanazed 7 and 30 days. NADPH diaphorase staining revealed a significant decrease in nitric oxide synthase (NOS) containing nerve fibers in the dorsal and intracavernosal nerves in all rats in the experimental group. Electron microscopy showed a variety of changes such as collapse of sinusoids, increased cell debris, fibroblast and myofibroblast loss, intracellular deposition of fat and collagen and fatty degeneration. RT-PCR revealed up-regulation of TGF-beta1 after 3 days but not after 7 days or 1 month. There is no significant difference in IGF-I or FGF expression between the experimental and control group. Bilateral ligation of internal iliac arteries produces a reliable animal model for traumatic arteriogenic ED. Further studies are needed to investigate the molecular mechanism of ED in this model.

中文翻译：

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创伤性动脉源性勃起功能障碍：大鼠模型。

我们开发了一种创伤性动脉源性勃起功能障碍（ED）的大鼠模型，用于研究血管生成性ED。作为实验组，对30只3个月大的雄性Sprague-Dawley大鼠进行内动脉的双侧结扎。对照组由12只大鼠经结扎而未结扎内动脉组成。在第3天，第7天和第1个月安乐死之前（实验组中有10只大鼠，对照组中有4只大鼠在每个时间点），通过电刺激海绵状神经来评估勃起功能。收集阴茎组织进行烟酰胺腺嘌呤二核苷酸磷酸（NADPH）心肌黄递酶染色，三色染色，电子显微镜和RT-PCR转化生长因子β（TGF-beta1），胰岛素样生长因子-I（IGF-1）和成纤维细胞生长因子（FGF）mRNA表达。3天和7天后，电刺激海绵状神经显示海绵体内压显着下降。1个月时未见勃起功能明显恢复。组织学显示所有实验大鼠的背神经纤维变性。安乐死7天和30天的实验大鼠的海绵体内平滑肌的体积几乎没有减少。NADPH心肌黄递酶染色显示，实验组中所有大鼠的背侧和海绵体神经中一氧化氮合酶（NOS）的神经纤维均明显减少。电子显微镜显示各种变化，例如正弦曲线的塌陷，细胞碎片增加，成纤维细胞和成肌纤维细胞的损失，脂肪和胶原的细胞内沉积以及脂肪变性。RT-PCR显示3天后TGF-beta1上调，但7天或1个月后没有上调。实验组和对照组之间的IGF-I或FGF表达没有显着差异。内动脉的双侧结扎为创伤性动员性ED产生了可靠的动物模型。需要进一步研究以研究该模型中ED的分子机制。