不对称二甲基精氨酸(ADMA)、对称二甲基精氨酸(SDMA)和l -精氨酸在动脉源性和非动脉源性勃起功能障碍患者中的作用

R. Paroni, A. Barassi, F. Ciociola, E. Dozio, E. Finati, I. Fermo, F. Ghilardi, G. M. Colpi, M. M. Corsi, G. V. Melzi d’Eril
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Diagnosis of erectile dysfunction was based on the International Index of Erectile Function Score and its aetiology was classified with penile echo-colour-Doppler in basal condition and after intracavernous injection of prostaglandin E1. The ADMA and SDMA concentrations were significantly higher in men with arteriogenic erectile dysfunction compared with those with erectile dysfunction of non-arteriogenic origin (<i>p </i>&lt; 0.05) and the concentrations in both subgroups were significantly higher than in controls (<i>p </i>&lt; 0.001). There was a negative correlation between ADMA and International Index of Erectile Function Score only in arteriogenic erectile dysfunction subgroup. L-arginine did not differ significantly neither between the two erectile dysfunction subgroups (<i>p </i>&gt; 0.05) nor between each of the two erectile dysfunction subgroups and controls (<i>p </i>&gt; 0.05). 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引用次数: 31

摘要

一氧化氮合酶抑制剂不对称二甲基精氨酸(ADMA)的血浆浓度与内皮功能障碍有关。我们研究了ADMA、对称二甲基精氨酸(SDMA)和l -精氨酸浓度与勃起功能障碍的关系。我们比较了61例动脉源性和非动脉源性勃起功能障碍的健康男性血浆ADMA、SDMA和l -精氨酸水平。根据国际勃起功能指数评分诊断勃起功能障碍,在基础状态和海绵内注射前列腺素E1后用阴茎回声彩色多普勒分类其病因。与非动脉源性勃起功能障碍男性相比,动脉源性勃起功能障碍男性的ADMA和SDMA浓度显著高于非动脉源性勃起功能障碍男性(p < 0.05),两亚组的浓度均显著高于对照组(p < 0.001)。ADMA与国际勃起功能指数评分仅在动脉源性勃起功能障碍亚组呈负相关。l -精氨酸在两个勃起功能障碍亚组之间没有显著差异(p > 0.05),在两个勃起功能障碍亚组和对照组之间也没有显著差异(p > 0.05)。动脉源性勃起功能障碍亚组l -精氨酸/ADMA和l -精氨酸/SDMA比值均显著低于对照组(p < 0.05)和非动脉源性勃起功能障碍患者(p < 0.05);非动脉源性勃起功能障碍患者的这两个比值与对照组没有差异(p > 0.05)。我们得出结论,与非动脉源性勃起功能障碍患者和对照组相比,动脉源性勃起功能障碍患者的ADMA和SDMA浓度显著升高,l -精氨酸/ADMA比值显著降低。ADMA与勃起功能障碍严重程度之间的负相关仅存在于动脉源性勃起功能障碍患者中。本研究支持区分动脉源性和非动脉源性勃起功能障碍患者的重要性,以研究导致勃起功能障碍的复杂勃起机制,并为动脉源性勃起功能障碍患者提供潜在的治疗药物。
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Asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA) and L-arginine in patients with arteriogenic and non-arteriogenic erectile dysfunction

The plasma concentration of asymmetrical dimethylarginine (ADMA), an inhibitor of nitric oxide synthase, has been linked to endothelial dysfunction. We investigated the relation between ADMA, symmetric dimethylarginine (SDMA) and L-arginine concentrations and erectile dysfunction. We compared plasma levels of ADMA, SDMA and L-arginine in 61 men in good health with erectile dysfunction of arteriogenic and non-arteriogenic origin. Diagnosis of erectile dysfunction was based on the International Index of Erectile Function Score and its aetiology was classified with penile echo-colour-Doppler in basal condition and after intracavernous injection of prostaglandin E1. The ADMA and SDMA concentrations were significantly higher in men with arteriogenic erectile dysfunction compared with those with erectile dysfunction of non-arteriogenic origin (p < 0.05) and the concentrations in both subgroups were significantly higher than in controls (p < 0.001). There was a negative correlation between ADMA and International Index of Erectile Function Score only in arteriogenic erectile dysfunction subgroup. L-arginine did not differ significantly neither between the two erectile dysfunction subgroups (p > 0.05) nor between each of the two erectile dysfunction subgroups and controls (p > 0.05). The L-arginine/ADMA and the L-arginine/SDMA ratios in arteriogenic erectile dysfunction subgroups were significantly lower than both in controls (p < 0.05) and in non-arteriogenic erectile dysfunction patients (p < 0.05); the two ratios in non-arteriogenic erectile dysfunction patients did not differ from those in the controls (p > 0.05). We conclude that ADMA and SDMA concentrations are significantly higher and L-arginine/ADMA ratio lower in patients who have arteriogenic erectile dysfunction compared with both patients with non-arteriogenic erectile dysfunction and controls. The negative correlation between ADMA and severity of erectile dysfunction is present only in patients with arteriogenic erectile dysfunction. This study supports the importance to always distinguish arteriogenic from non-arteriogenic erectile dysfunction patients to study the complicate erectogenic mechanisms that lead to erectile dysfunction and also to provide potential therapeutic agents for patients with arteriogenic erectile dysfunction.

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