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目的 探讨糖尿病（ＤＭ） 性阴茎勃起功能障碍（ＥＤ） 的发病机理。 方法 ＳＤ 大鼠注射链脲佐菌素制造ＤＭ 动物模型后，注射阿朴吗啡观察６ 周、８ 周及１２ 周大鼠阴茎勃起情况，筛选ＤＭ 性ＥＤ 大鼠模型，观察其阴茎海绵体组织超微结构的改变。 结果 ＤＭ 性ＥＤ 大鼠模型阴茎海绵体内皮细胞及平滑肌细胞超微结构均有明显的病理改变：线粒体退变、内质网扩张，糖原颗粒、吞饮小泡及微丝减少。此外，还可见大量间质组织增生及微血管腔闭塞。随ＤＭ 病程不同，其改变程度不同，８ 周时以内皮细胞损害为明显，１２ 周时以平滑肌细胞损害为明显。 结论 ＤＭ 严重影响阴茎勃起功能，海绵体组织超微结构的病理改变可能是ＤＭ 性ＥＤ 发病机理之一。
Objective To investigate the pathogenesis of diabetic penile erectile dysfunction (ED). Methods SD rats were injected with streptozotocin to make animal model of DM. Apomorphine was injected into the rats for 6 weeks, 8 weeks and 12 weeks to observe the penile erection. Microstructure changes. Results The ultrastructure of endothelial cells and smooth muscle cells of penile corpus cavernosum in DM rats showed obvious pathological changes: degeneration of mitochondria, expansion of endoplasmic reticulum, reduction of glycogen granules, swallow vesicles and microfilaments. In addition, we can see a large number of interstitial tissue hyperplasia and microvascular occlusion. With the different duration of DM, the degree of change is different, 8 weeks to endothelial cell damage was obvious, 12 weeks to smooth muscle cell damage was obvious. Conclusion DM has a serious effect on erectile function. The pathological changes of spontaneous ultrastructure may be one of the pathogenesis of DM.