Alternative Medicine

Hypercholesterolemia

Hypercholesterolemia and subsequent atheroscle-rosis are well-recognized risk factors for the devel-opment of vasculogenic ED. Viagra online in Australia Rarely is hypercholesterolemia-associated ED in men seen in isolation, without other risk factors such as obesity, smoking, age, and diabetes. Rabbits are the most used species in hypercholesterolemia. A high cholesterol/high triglyceride diet, sometimes com-bined with balloon injury of the aortoiliac arteries, is used to induce atherosclerotic plaques in the arterial supply to the penis. This results in the impairment of endothelium-dependent cavernosal smooth muscle relaxation and agonist-induced penile erection with papaverine. These defects could not be explained solely by the occlusion of blood flow, but were also accompanied by defects in smooth muscle signaling.

Cavernous Nerve Injury

Due to the high prevalence of ED following pelvic surgery as a result of injury to the neurovascular bundle, there has been a great interest in models of cavernous injury. The goal is to identify the mechanisms leading to the ED (e.g., penile apotosis and fibrosis), as well as identifying meth-ods of preventing these pathological changes or remediating them. The most widely used animal model of cavernous nerve injury (CNI) is the cav-ernous nerve-injured rat model. Injury can be induced by crush, cut or freezing rat models. Through a lower abdominal midline incision, the posterolateral area of the prostate is exposed on both sides and the major pelvic ganglions and cavernous nerves are identified. The cavernous nerves, unilaterally or bilaterally, are either sharply divided with knives to remove a segment of nerve, cauterized, or frozen using a thermocouple. ED-observed postradical prostatectomy is most likely attributed to changes in the endothelium and smooth muscle cells from a loss in neural integrity. The absence of neural input to the penis after CNI in the rat results in cavernosal smooth muscle apoptosis, alterations in the endothelium and smooth muscle function, decrease in neuronal NOS nerve fibers in the penis, pelvic ganglia, and fibrosis. The CNI rat model has led to a more thorough understanding of the pathophysiological sequences involved in the development of postradical prostatectomy ED.

Hypogonadism Canadian Health Care mall

Androgens are necessary for the maintenance of the mammalian erectile response. In most animals, androgens are essential in maintaining sexual behavior. However, evidence shows that androgens are also necessary to maintain the erectile apparatus of the penis. Effects of castration on sexual function are evaluated by the observation of copulatory behaviors, penile reflex, and erectile response electrical stimulation of the cavernous nerve. Particularly in the rat model, androgens act centrally to support copulatory behavior and peripherally to maintain constitutive NOS activity and support the veno-occlusive mechanisms. Thus, the erectile response in the rat is androgen dependent. Castrated rats have been used as models to study venoocclusive dysfunction because cavernosal sinusoidal smooth muscle fails to fully relax and blood flow continues during erection in castrated rats, suggesting the failure of venoocclusion. Despite these reports of the importance of androgens in the erectile response of laboratory animals, the role of androgens in the maintenance of the human erectile response remains controversial. Even in severely hypogonadal men, the erectile response is not always lost. Therefore, the hypogonadal animal model of ED may be best utilized as a model of venoocclusive ED.

Conclusions

A large number of models exist for the study of male sexual function. Each model has both strengths and limitations. Care must always be taken before extrapolating too quickly from experimental data to a seemingly parallel clinical situation. Practical considerations have led to a great reliance on rodent models viagra in Canada. These have the advantage of cost, ease of handling, and a large foundation of biological knowledge. There are rodent models for examining every aspect of penile erection from higher neural control down to molecular events within the erectile tissue. The disadvantage of rodent models is that they do not always accurately reflect human physiology and pathophysiology, although they seem to share many basic mechanisms. Therefore, the validation of any given model must be assessed for a particular application. The utility of these models is amply demonstrated by the great expansion of our understanding of male sexual physiology in recent years. Future challenges will be to develop more models of pathophysiological conditions.