Azadzoi K M, Saenz de Tejada I
Department of Urology, Boston University Medical Center, Massachusetts.
J Urol. 1992 Nov;148(5):1587-91. doi: 10.1016/s0022-5347(17)36975-6.
The effect of alloxan-induced diabetes on the reactivity of corporeal nerves, endothelium and smooth muscle was studied in the New Zealand white rabbit. Fifteen rabbits were randomly divided into treated (n = 6) and control (n = 9) groups. The treated group was maintained for 6 weeks. Two control groups were studied. One control group (n = 3) was maintained for 6 weeks as littermate controls for diabetic group. The second control group (n = 6) was not maintained but was weight matched with the 6 week diabetic group. The reactivity of corpus cavernosum tissue from the diabetic animals and the control animals was studied in organ chambers. When tissue contraction was produced with phenylephrine for the study of relaxation to various stimuli, the tension induced was similar in the diabetic and the control groups. Relaxation of corpus cavernosum tissue to electrical stimulation of autonomic nerves as well as relaxation to the endothelium-dependent vasodilator acetylcholine were comparably unaffected in the weight matched and littermate control groups while significantly inhibited in the diabetic group. Treatment of the corporeal tissue with the cyclooxgenase inhibitor indomethacin enhanced the relaxation to electrical stimulation and to acetylcholine in the control and in the diabetic groups but did not improve the significant difference in relaxation between the two groups. Relaxation of corporeal tissue to endothelium-independent vasodilators, papaverine and nitroprusside was similar in the control groups and the diabetic groups. It is concluded that diabetes impairs neurogenic and endothelium-mediated relaxation of rabbit corpus cavernosum smooth muscle. These findings are comparable to those described in corpus cavernosum tissue from diabetic men, showing the validity of this experimental animal model. The mechanism for the nerve or endothelial dysfunction does not appear to involve alteration in cyclooxygenase products of arachidonate or the ability of the corporeal smooth muscle to relax via a cGMP-dependent mechanism. Since nitric oxide has been shown to act as the nonadrenergic noncholinergic neurotransmitter as well as endothelium-derived relaxing factor (EDRF) of the trabecular smooth muscle, it is possible that impairment of neurogenic and endothelium-dependent relaxation due to diabetes is mediated by alteration in the synthesis or availability of nitric oxide in corporeal tissue.
在新西兰白兔中研究了四氧嘧啶诱导的糖尿病对阴茎神经、内皮和平滑肌反应性的影响。15只兔子被随机分为治疗组（n = 6）和对照组（n = 9）。治疗组维持6周。研究了两个对照组。一个对照组（n = 3）作为糖尿病组的同窝对照维持6周。第二个对照组（n = 6）不维持，但体重与6周糖尿病组匹配。在器官腔室中研究了糖尿病动物和对照动物阴茎海绵体组织的反应性。当用去氧肾上腺素引起组织收缩以研究对各种刺激的舒张时，糖尿病组和对照组诱导的张力相似。在体重匹配组和同窝对照组中，阴茎海绵体组织对自主神经电刺激的舒张以及对内皮依赖性血管舒张剂乙酰胆碱的舒张同样未受影响，而在糖尿病组中则显著受到抑制。用环氧化酶抑制剂吲哚美辛处理阴茎组织可增强对照组和糖尿病组对电刺激和乙酰胆碱的舒张，但并未改善两组之间舒张的显著差异。阴茎组织对非内皮依赖性血管舒张剂罂粟碱和硝普钠的舒张在对照组和糖尿病组中相似。结论是糖尿病损害了兔阴茎海绵体平滑肌的神经源性和内皮介导的舒张。这些发现与糖尿病男性阴茎海绵体组织中描述的发现相当，表明该实验动物模型的有效性。神经或内皮功能障碍的机制似乎不涉及花生四烯酸环氧化酶产物的改变或阴茎平滑肌通过cGMP依赖性机制舒张的能力。由于一氧化氮已被证明是小梁平滑肌的非肾上腺素能非胆碱能神经递质以及内皮源性舒张因子（EDRF），因此糖尿病导致的神经源性和内皮依赖性舒张受损可能是由阴茎组织中一氧化氮的合成或可用性改变介导的。
