模拟分娩产伤及绝经建立女性生殖器性唤起障碍大鼠模型及阴道微血管损害的致病机制研究

我国女性性唤起障碍发病率高达21.5%，分为主观和生殖器性唤起障碍。女性生殖器性唤起障碍（FGSAD）是指性器官的器质性病变，包括性器官敏感性的降低、阴道充血、松弛、滑润及阴蒂充血膨胀障碍等，其中阴道病变最为常见。因缺乏可靠的动物模型，已成为FGSAD研究和治疗的瓶颈。临床发现FGSAD在阴道产伤和绝经女性发病率较高，因此，其病因可能为阴道损伤和雌激素撤退最为重要。前期实验通过模拟女性分娩产伤及绝经生理过程构建动物模型，发现其阴道血流，收缩功能和组织学发生显著改变，符合FGSAD阴道病理变化。因此，本研究通过优化不同处理方式，利用阴道血流测定和组织学评估该FGSAD大鼠模型建立的最佳时间和方式，建立标准化FGSAD大鼠模型。目前FGSAD的致病机制不清楚，前期发现该模型阴道微血管显著减少。我们通过检测VEGF相关血管信号通路，明确FGSAD阴道组织微血管损害的致病机制。

The incidence of female sexual arousal disorder is up to 21.5%. There are subjective and genital sexual arousal disorders. Female genital arousal disorder (FGSAD) refers to the organic organs of the organic lesions, including the reduction of sexual organs, vaginal congestion, relaxation, smoothness and clitoris congestion swelling disorders, of which the most common vaginal lesions. But the lack of clinical specimens and a standard animal model has become the limitation of FGSAD research and treatment. FGSAD may cause by genital injury combined hormone withdrawal. Previously,by simulating birth trauma of the female prolonged second stage and menopause physiological processes, we found that vaginal blood flow, contraction function and histology have changed dramatically which accords with the physiological changes of FGSAD, validated our hypothesis . Therefore, through the optimization of different processing methods to establish the rat model of FGSAD and evaluation of the best time and way by the rat model for arousal vaginal response, vaginal contraction function and histopathological techniques. Currently FGSAD pathogenic mechanism is unclear. Previous our study also found that the microvasculars of vaginal tissue were significantly reduced and VEGF decline in FGSAD. Therefore, we use molecular biology technology to understand the change of VEGF signaling pathway related artery and clear the pathogenic mechanisms of vaginal microvascular in FGSAD.