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糖尿病性勃起功能障碍 (ED)的发病机制尚未完全阐明 ,除神经病变和血管病变的作用外 ,糖尿病还通过降低一氧化氮合酶 (NOS)活性、糖基化终末产物 (AGEs)和氧自由基灭活一氧化氮 (NO)等途径引起局部NO水平降低 ,细胞内cGMP浓度下降 ,导致海绵体平滑肌舒张性减弱 ;还使海绵体内皮素 1浓度升高 ,平滑肌收缩性增强 ;同时也引起海绵体勃起组织结构改变、平滑肌数量减少 ,协同导致糖尿病性ED的发生。另外 ,糖尿病引起的低雄激素水平可能也在其中起一定作用。
The pathogenesis of diabetic erectile dysfunction (ED) has not yet been fully elucidated. In addition to the role of neuropathy and vascular disease, diabetes also reduces nitric oxide synthase (NOS) activity, advanced glycation end products (AGEs) and oxygen Free radical inactivation of nitric oxide (NO) and other pathways cause local NO levels decreased, decreased intracellular cGMP concentration, leading to relaxation of spontaneous smooth muscle relaxation; also make cavernous endothelin 1 concentration, smooth muscle contraction increased; also Cause sponge erectile tissue structure changes, reduce the number of smooth muscle, synergistically lead to the occurrence of diabetic ED. In addition, low androgen levels caused by diabetes may also play a role in this.