VASCULOGENIC FEMALE SEXUAL DYSFUNCTION - THE HEMODYNAMIC BASIS FOR VAGINAL ENGORGEMENT INSUFFICIENCY AND CLITORAL ERECTILE INSUFFICIENCY

Objective: Organic female sexual dysfunction may be related in part to vasculogenic impairment of the hypogastric-vaginal/clitoral arterial bed. The aim was to develop an animal model of vaginal engorgement ins ufficiency and clitoral erectile insufficiency. Methods: pelvic nerve stimulated vaginal engorgement and clitoral erection were achieved in control (normal diet, n=8) and atherosclerotic (balloon injury of aort o-iliac arteries and 0.5% cholesterol diet, n=7) New Zealand White fem ale rabbits. After 16 weeks, novel hemodynamic variables including vag inal wall and clitoral blood now, vaginal wall and clitoral intracaver nosal pressure, vaginal length, vaginal luminal pressure, blood levels of cholesterol and triglycerides, aorto-iliac angiography and vaginal wall and clitoral erectile tissue histology were recorded in the two groups. Results: Concerning pelvic nerve stimulated vaginal hemodynami c changes, there was significantly less increase in blood now (ml/min/ 100 gm tissue), wall pressure (mmHg) and length changes (mm) in athero sclerotic (9.3 +/- 3.7, 4.8 +/- 3.8, 67.3 +/- 8.3) compared to control (13.9 +/- 4.5, 5.5 +/- 2.6, 74.1 +/- 10.0) animals respectively. Hist ologic examination of clitoral erectile tissue demonstrated cavernosal artery atherosclerotic changes and diffuse vaginal and clitoral fibro sis. Aorto-iliac angiography in atherosclerotic animals revealed diffu se moderate to severe atherosclerotic occlusion. Conclusions: Vaginal engorgement and clitoral erection depend on increased blood inflow. At herosclerosis is associated with vaginal engorgement insufficiency and clitoral erectile insufficiency.