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Ultrastructural changes of penile cavernous tissue in multiple sclerotic rats.

机译:多发性硬化大鼠阴茎海绵体组织的超微结构变化。

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INTRODUCTION: Multiple sclerosis (MS) is one of the important risk factors resulting in erectile dysfunction (ED). The ultrastructure of corpus cavernous of the penis have an important role in the mechanism of erection. AIM: It is suggested that different medical conditions produce similar degenerative tissue responses. We investigated the ultrastructural changes of penile cavernous tissue and its association with ED in multiple sclerotic rats. METHODS: After induction of multiple sclerosis in rat, maximum intracavernosal pressure/mean arterial pressure (ICP(max)/MAP) in the severity multiple sclerotic rats (group A),moderate multiple sclerotic rats (group C), and age-matched control rat (group B) were observed and compared. The ultrastructure of the penile cavernous tissue was studied by transmission electron microscope. Expression of neuronal nitric oxide synthase (nNOS) in penile tissue were examined immunohistochemically. MAIN OUTCOME MEASURES: Severity MS (score 3) not only significantly decrease the ICPmax/MAP x 100 and the expression of nNOS, but also might affect the ultrastructure of the penis. RESULTS: The ICP(max)/MAP x 100 in group A was significantly less than in group B and group C at 3 V (5.65 +/- 1.78, 20.49 +/- 5.84, and 12.78 +/- 5.76, respectively) and at 5 V (6.70 +/- 1.39, 23.66 +/- 5.19, and 16.95 +/- 3.31, respectively) stimulation voltage, respectively (P < 0.05). Significant ultrastructral pathological changes characterized by degeneration and demyelination singularly in Schwann cells without significant ultrastructural change of smooth muscle cells and endothelium cells were observed in penile cavernous tissue of group A rats. CONCLUSIONS: The function of penile erection is affected by MS, and the ultrastructural pathological changes of the penile cavernous tissue may be one of the important mechanisms of ED caused by severity MS.
机译:简介:多发性硬化症(MS)是导致勃起功能障碍(ED)的重要危险因素之一。阴茎海绵体的超微结构在​​勃起机制中具有重要作用。目的:建议不同的医学状况产生相似的变性组织反应。我们调查了多发性硬化大鼠中阴茎海绵体组织的超微结构变化及其与ED的关系。方法:在诱发多发性硬化症后,严重程度为多发性硬化症的大鼠(A组),中度多发性硬化症的大鼠(C组)和年龄匹配的对照组的最大海绵体内压力/平均动脉压(ICP(max)/ MAP)观察并比较大鼠(B组)。用透射电子显微镜研究了阴茎海绵体组织的超微结构。免疫组织化学检查神经元一氧化氮合酶(nNOS)在阴茎组织中的表达。主要观察指标:严重程度MS(评分3)不仅显着降低ICPmax / MAP x 100和nNOS的表达,还可能影响阴茎的超微结构。结果:在3 V电压下,A组的ICP(max)/ MAP x 100显着低于B组和C组(分别为5.65 +/- 1.78、20.49 +/- 5.84和12.78 +/- 5.76)和在5 V(分别为6.70 +/- 1.39、23.66 +/- 5.19和16.95 +/- 3.31)刺激电压下(P <0.05)。在A组大鼠的阴茎海绵状组织中观察到明显的特征为雪旺细胞变性和脱髓鞘的特征性超微结构改变,而平滑肌细胞和内皮细胞无明显超微结构改变。结论:MS对阴茎勃起功能有影响,而阴茎海绵体组织的超微结构病理改变可能是严重MS引起ED的重要机制之一。

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