Our clinical data enabled us to demonstrate a correlation between impaired lipid metabolism and vasculogenic impotent men. Our aim was to evaluate the effect of an impaired lipid metabolism on the smooth muscle of the corpus cavernosum. A total of 16 rabbits were given a cholesterol-enriched diet for 3 months, and 8 of these received additional thromboxane A2 receptor antagonist; 10 other rabbits (control) were fed a normal diet. Subsequently, cavernous tissue biopsies were taken, and tissue lipid extractions and electron microscopic evaluation were made from 3 rabbits in each group. In the untreated high-cholesterol diet group, cholesterol levels reached approx. 2.1 micrograms/mg body weight compared with 1.07 micrograms/mg b.wt. in the thromboxane A2 receptor antagonist-treated group and elevated levels compared with control group. Similar results were found for the triglyceride and free fatty acid levels. Lecithin tissue levels in treated rabbits were distinctly elevated against those of other 2 groups. Ultramorphological examination of the control group disclosed normal smooth muscle cell (SMC) architecture with numerous sites of intercellular contacts. These findings contrasted with those of the high-cholesterol diet groups which showed significant SMC degeneration with loss of intercellular contacts. Our data imply that impaired lipid metabolism causes cavernous SMC degeneration which plays a major role in the pathogenesis of erectile dysfunction. The thromboxane A2 receptor antagonist seems to produce a protective metabolic effect on the erectile tissue which may have some consequences future treatment strategies.

In 6 dogs and 6 monkeys electrical stimulation of the cavernous, pudendal and hypogastric nerve was performed to gain better understanding of the erectile neurophysiology. Arterial flow, intracorporeal pressure and venous restriction studies during single and combined neurostimulation demonstrated that initiation and maintenance of erection is a parasympathetic phenomenon. Penile rigidity however, could only be achieved with additional pudendal nerve stimulation resulting in muscular compression of the blood distended cavernous bodies. Detumescence or subsidence of erection is primarily under sympathetic control, due to inhibition of sinusoidal smooth muscle relaxation. On the basis of our observations we conclude that penile erection is dependent upon three neurophysiological mechanisms: 1. the parasympathetic "vascular mechanism", the somatomotor "muscular mechanism" and the sympathetic "inhibitory mechanism".

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