Erectile impotence afflicts between ten and fourteen million men in the United States. Vasculogenic impotence is the most frequent cause of organic impotence and is estimated to exist in over five million American men. At present hemodynamic data relating penile erection and arterial inflow in abnormal pelvic hemodynamic states is lacking. As a result therapeutic options in vasculogenic impotence are severely restricted. It is the aim of this study to define the hemodynamic mechanisms responsible for vasculogenic impotence and to determine the effectiveness of three treatment forms, transluminal angioplasty, microvascular surgery and vasodilator therapy, in established experimental animal models. In particular, an objective evaluation is needed to assess transluminal angioplasty for the treatment of vasculogenic impotence. Transluminal angioplasty is already being used effectively to restore arterial inflow in similar sized atherosclerotic vessels in the coronary circulation without the need for surgery. The first animal model is developed by placing controlled mechanical restrictions in various locations within the hypogastric-cavernous arterial bed. Acute and chronic studies will be performed to define critical inflow levels for penile erection, to determine if unilateral restriction can result in penile erection and to assess if during chronic obstruction pelvic collateral circulation is adequate to restore critical arterial inflow. The second animal model is created by inducing segmental atherosclerosis within the hypogastric-cavernous arterial bed by the Baumgartner technique followed by feeding of an atherogenic diet. The consequences of altered pelvic hemodynamics in either model is assessed by recording arterial inflow, corporal body pressure and pressure above and below the occlusion during pelvic nerve stimulation. The three treatment options will be performed in both chronic models and the efficacy of restored pelvic blood flow and penile erection evaluated during subsequent pelvic nerve stimulation. Comprehending the role of arterial hemodynamic factors in vasculogenic impotence is necessary so that maximum therapeutic benefit may be realized by the large numbers of patients afflicted with this syndrome.
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NIH ExPorter