Vasculogenic female sexual dysfunction: The hemodynamic basis for vaginal engorgement insufficiency and clitoral erectile insufficiency

Abstract

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 insuf®ciency and clitoral erectile insuf®ciency.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¯ow, 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 signi®cantly less increase in blood¯ow (ml/min/100 gm tissue), wall pressure (mmHg) and length changes (mm) in atherosclerotic (9.3 AE 3.7, 4.8 AE 3.8, 67.3 AE 8.3) compared to control (13.9 AE 4.5, 5.5 AE 2.6, 74.1 AE 10.0) animals respectively. Histologic examination of clitoral erectile tissue demonstrated cavernosal artery atherosclerotic changes and diffuse vaginal and clitoral ®brosis. Aorto-iliac angiography in atherosclerotic animals revealed diffuse moderate to severe atherosclerotic occlusion.Conclusions: Vaginal engorgement and clitoral erection depend on increased blood in¯ow. Atherosclerosis is associated with vaginal engorgement insuf®ciency and clitoral erectile insuf®ciency.

Decreased circulating levels of estrogen alter vaginal and clitoral blood flow and structure in the rabbit

“…In our previous studies we utilized a similar technique in the rabbit model and found that vaginal blood ow in the muscular layer of the vaginal wall in the quiescent vaginal state was 5.9 AE 2.6 mlamina100 g tissue. 7 We also found that blood¯ow in the muscular layer of the vagina increased to 13.9 AE 4.5 mlamina100 g during nerve stimulationinduced vaginal engorgement. 7 This would suggest that vaginal blood¯ow in the mucosal layer of the vagina is much greater compared with blood¯ow in the muscular layer in the quiescent vaginal state as well as during engorgement.…”

“…7 We also found that blood¯ow in the muscular layer of the vagina increased to 13.9 AE 4.5 mlamina100 g during nerve stimulationinduced vaginal engorgement. 7 This would suggest that vaginal blood¯ow in the mucosal layer of the vagina is much greater compared with blood¯ow in the muscular layer in the quiescent vaginal state as well as during engorgement. Oophorectomyinduced decrease in the circulating levels of estrogen adversely affected vaginal mucosal blood¯ow.…”

“…2 In our previous studies with the rabbit model, we found that the development of vaginal and clitoral engorgement depends on an adequate increase in the vaginal wall and clitoral intracavernosal blood ows. 7 We also found that occlusive disease of the iliac and pudendal arteries reduced arterial in¯ow to the vagina and clitoris and impaired vaginal and clitoral engorgement. 7 Studies with a rat model showed that estrogen withdrawal resulted in vaginal atrophy, intramural collagen accumulation and structural changes in vaginal wall microvasculature.…”

“…7 We also found that occlusive disease of the iliac and pudendal arteries reduced arterial in¯ow to the vagina and clitoris and impaired vaginal and clitoral engorgement. 7 Studies with a rat model showed that estrogen withdrawal resulted in vaginal atrophy, intramural collagen accumulation and structural changes in vaginal wall microvasculature. 8 These structural changes were shown to diminish by estrogen replacement therapy.…”

Nitrergic neurotransmission mediates the non‐adrenergic non‐cholinergic responses in the clitoral corpus cavernosum of the rabbit

“…Although the number of studies investigating the pathophysiology of female sexual dysfunction is signi®cantly lower than those of male erectile dysfunction (Levin, 1992), the studies that do exist suggest that a de®ciency in clitoral tumescence may be important in female sexual dysfunction (Levin, 1980, Park et al, 1997. Sildena®l, an inhibitor of type V cyclic GMP phosphodiesterase, has been shown to be e ective in the treatment of male erectile dysfunction (Boolell et al, 1996).…”