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目的:观察不同吸烟量大鼠阴茎血管内皮细胞P-选择素的表达和海绵体超微结构的改变,初步探讨吸烟导致阴茎勃起功能障碍的发病机制。方法:健康Wistar大鼠50只,随机均分为正常对照组、长期大量吸烟组、长期小量吸烟组、短期大量吸烟组和戒烟组。皮下注射阿朴吗啡(APO)检测阴茎勃起功能。采用ELISA法测定大鼠阴茎血管内皮细胞P-选择素的水平,透射电镜观察大鼠阴茎海绵体超微结构的变化。结果:正常对照组P-选择素为(10.78±1.71)ng/L;长期大量吸烟组为(62.62±5.95)ng/L;长期小量吸烟组为(40.06±3.97)ng/L;短期大量吸烟组为(41.37±4.06)ng/L;戒烟组为(22.80±3.15)ng/L。4组与对照组比较均有显著性差异(P<0.05)。电镜观察吸烟各组内皮细胞、血窦、平滑肌细胞分布杂乱,血管内皮细胞连续性破坏;内皮细胞和平滑肌细胞超微结构被破坏。大量间质组织增生、纤维化。结论:吸烟可致阴茎血管内皮细胞P-选择素表达增加,破坏海绵体组织超微结构,可能是吸烟致阴茎勃起功能障碍的主要途径之一。
PURPOSE: To observe the changes of P-selectin and ultrastructure of corpus cavernosum in penile vascular endothelial cells of different cigarette smokers and to explore the pathogenesis of erectile dysfunction caused by smoking. Methods: Fifty healthy Wistar rats were randomly divided into normal control group, long-term heavy smoking group, long-term small smoking group, short-term heavy smoking group and smoking cessation group. Subcutaneous injection of apomorphine (APO) to detect penile erection. The levels of P-selectin in rat penile vascular endothelial cells were measured by ELISA and the ultrastructure of rat penis were observed by transmission electron microscope. Results: P-selectin was (10.78 ± 1.71) ng / L in the control group, (62.62 ± 5.95) ng / L in the long-term heavy smoking group and (40.06 ± 3.97) ng / L in the long- The smoking group was (41.37 ± 4.06) ng / L, while the smoking cessation group was (22.80 ± 3.15) ng / L. There were significant differences between the 4 groups and the control group (P <0.05). Electron microscopy showed that the distribution of endothelial cells, sinusoids and smooth muscle cells was disordered and the vascular endothelial cells were destroyed continuously in the smoking groups. The ultrastructure of endothelial cells and smooth muscle cells were destroyed. A large number of interstitial tissue proliferation, fibrosis. CONCLUSIONS: Smoking can increase the expression of P-selectin in penile vascular endothelial cells and destroy the ultrastructure of sponge tissue, which may be one of the main ways of smoking-induced erectile dysfunction.