Diabetes and male sexual function (Part 3)
Acute hyperglycemia alone may induce endothelial dysfunction and also decrease the velocity of nerve conduction in rodents. Chronic hyperglycemia is associated with the loss of myelinated and unmyelinated fibres and attenuated nerve fibre regeneration. Diffuse abnormalities of the peripheral nerve vasculature (vasa nervosum) are well documented in diabetics. In the late stages of diabetes — buy diabetes drugs, there may be complete vascular occlusion with atherosclerosis, thickening of capillary basement membrane, dilation and microaneurysms of capillaries as well as endothelial hyperplasia, and desquamation and degeneration of pericytes. These lesions induce a microangiopathy that leads to endoneurial hypoxia and demyelination. The lesions decrease the blood flow to the vaso nervosum and, thus, lead to nerve ischemia. A peripheral neuropathy then develops, which initially affects small unmyelinated fibres. Around 61.2% of diabetics who present with impotence show evidence of neuropathy.
In erectile tissue, there is atrophy of the smooth muscle cells and lipid deposition in the corpus cavernosum. Urogenital nerves also show morphological alterations, nerve conduction is impaired and neurotransmitter levels are altered. Vasoactive intestinal polypeptide immunoreactivity, and acetylcholine synthesis and release have been shown to be reduced in nerves from diabetic patients. In the penis, smooth muscle shows impaired neurogenic and endothelium-dependent relaxation. The dorsal nerve of the penis is involved in erectile response. In diabetics, the conduction velocity of the dorsal nerve is significantly slower than that in normal males and can be demonstrated with the bulbocavernous reflex. Unfortunately, differences in bulbocavernous reflex latency are not useful for differentiating diabetics from nondiabetics. Autonomic nerve testing is found to be abnormal in 63% of patients with diabetic ED.