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Increased endothelial apoptotic cell density in human diabetic erectile tissue--comparison with clinical data.

机译:人糖尿病勃起组织中内皮细胞凋亡细胞密度增加-与临床数据比较

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INTRODUCTION: Erectile dysfunction (ED) is a common complication of diabetes. Endothelial cell (EC) dysfunction is one of the main mechanisms of diabetic ED. However, loss of EC integrity has never been assessed in human diabetic corpus cavernosum. AIM: To identify and quantify apoptotic cells in human diabetic and normal erectile tissue and to compare these results with each patient's clinical data and erection status. METHODS: Eighteen cavernosal samples were collected, 13 from diabetics with ED and 5 from nondiabetic individuals. Cavernosal structure and cell proliferation status were evaluated by immunohistochemistry. Tissue integrity was assessed by terminal transferase dUTP nick end labeling assay, an index of apoptotic cell density (ACD) established and compared with each patient age, type of diabetes, arterial risk factors number, arterial/veno-occlusive disease, response to intracavernous vasoactive injections (ICI), and penile nitric oxide release test (PNORT). MAIN OUTCOME MEASURES: Establish an index of ACD and correlate those results with patient clinical data. RESULTS: Nondiabetic samples presented few scattered cells in apoptosis and an ACD of 7.15 +/- 0.44 (mean apoptotic cells/tissue area mm(2) +/- standard error). The diabetic group showed an increased ACD of 23.82 +/- 1.53, and apoptotic cells were located specifically at vascular sites. Rehabilitation of these endothelial lesions seemed impaired, as no evidence of EC proliferation was observed. Furthermore, higher ACD in diabetic individuals correlated to poor response to PNORT and to ICI. CONCLUSIONS: We provided evidence for the first time that loss of cavernosal EC integrity is a crucial event involved in diabetic ED. Furthermore, we were able to establish a threshold between ACD values and cavernosal tissue functionality, as assessed by PNORT and vasoactive ICI.
机译:简介:勃起功能障碍(ED)是糖尿病的常见并发症。内皮细胞(EC)功能障碍是糖尿病性ED的主要机制之一。然而,从未在人类糖尿病体海绵体中评估EC完整性的丧失。目的:鉴定和量化人类糖尿病和正常勃起组织中的凋亡细胞,并将这些结果与每位患者的临床数据和勃起状态进行比较。方法:收集了18个海绵体样本,其中13例来自患有ED的糖尿病患者,另外5例来自非糖尿病患者。通过免疫组织化学评估海绵体结构和细胞增殖状态。通过末端转移酶dUTP缺口末端标记测定法评估组织完整性,建立凋亡细胞密度指数(ACD)并与每个患者的年龄,糖尿病类型,动脉危险因素数目,动脉/静脉闭塞性疾病,对海绵体内血管活性的反应进行比较注射(ICI)和阴茎一氧化氮释放测试(PNORT)。主要观察指标:建立ACD指数并将这些结果与患者临床数据相关联。结果:非糖尿病患者的细胞凋亡中散在的细胞很少,ACD为7.15 +/- 0.44(平均凋亡细胞/组织面积mm(2)+/-标准误差)。糖尿病组显示ACD增加至23.82 +/- 1.53,并且凋亡细胞专门位于血管部位。这些内皮损伤的修复似乎受损,因为未观察到EC增殖的迹象。此外,糖尿病患者中较高的ACD与对PNORT和ICI的不良反应相关。结论:我们首次提供证据表明海绵体EC完整性的丧失是糖尿病性ED涉及的关键事件。此外,通过PNORT和血管活性ICI评估,我们能够在ACD值和海绵体组织功能之间建立阈值。

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