肝郁证勃起功能障碍大鼠模型建立的实验研究

Experimental research on the establishment of rat model with erection dysfunction due to stagnation of the liver-qi

目的建立大鼠肝郁证勃起功能障碍(ED)模型,揭示肝郁证ED的可能发病机制。方法采用束缚盒慢性应激法,逐渐增加束缚强度与时间,造模共50d,观测雄性大鼠性活动,包括嗅舔次数,首次爬背时间,爬背次数,累计爬背时间并制作性器官病理切片及检测阴茎组织一氧化氮合成酶等指标。结果大鼠性活动及体重均表现出明显的差异性。性器官病理切片显示正常对照组与模型组存在差异。一氧化氮合成酶正常对照组与模型组差异有显著性(P<0．05)。结论实验表明束缚盒慢性应激法可造成大鼠肝郁证ED,其发病机制一是肝郁大鼠阴茎组织一氧化氮合成酶降低,使介导阴茎勃起的最主要非胆碱能非肾上腺能神经递质NO产生减少,阻止海绵体平滑肌舒张;二是肝郁导致性器官组织细胞病理改变,因此无法完成正常的勃起功能。

Objective To establish the rat models of ED with stagnation of the liver-qi, in order to reveal the possible mechanism of ED. Methods The models of ED caused by stagnation of the liver-qi are established for 50 days by adopting the methods of bound chronic stress, gradually strengthening the bound intensity and prolonging its time, thus, causing the rats＇ stagnation of the liver-qi. Then, observing the male rats＇ sex activity, including licking-smelling times, the first back-climbing time, back-climbing frequency, accumulating back-climbing times. Pathological sections of sex organs and the index of NOS in penis were determined. Results Significant differences between the control group and the model groups could be seen in rats＇ sex activities and their body weight.and it is very different in pathological sections of sex organs and NOS （P〈0.05）. Conclusion The method of bound chronic stress can cause the rats＇ ED. The first pathogenesis. NOS in the penis of rats with stagnation of the liver-qi has been reduced, which causes the reduction of non-cholinergic and non-adrenergic transmitters and prevents the diastolization of cavernous smooth muscles; the second pathogenesis, the stagnation of the liver-qi may cause patlcogenic changes in cells of sex organs. Thus, they can not have normal erect function.