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 insufficiency 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 aorto-iliac arteries and 0.5% cholesterol diet, n = 7) New Zealand White female rabbits. After 16 weeks, novel hemodynamic variables including vaginal wall and clitoral blood flow, vaginal wall and clitoral intracavernosal 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 hemodynamic changes, there was significantly less increase in blood flow (ml/min/100 gm tissue), wall pressure (mmHg) and length changes (mm) in atherosclerotic (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. Histologic examination of clitoral erectile tissue demonstrated cavernosal artery atherosclerotic changes and diffuse vaginal and clitoral fibrosis. Aorto-iliac angiography in atherosclerotic animals revealed diffuse moderate to severe atherosclerotic occlusion.

CONCLUSIONS

Vaginal engorgement and clitoral erection depend on increased blood inflow. Atherosclerosis is associated with vaginal engorgement insufficiency and clitoral erectile insufficiency.