作者: Kazem M. Azadzoi , Tara A. Master , Mike B. Siroky
DOI: 10.1002/J.1939-4640.2004.TB02804.X
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摘要: Arterial occlusive disease is one of the leading causes organic erectile dysfunction (ED). Recent studies have shown that incidence cardiovascular closely correlates with prevalence ED. Also, ED thought to be an early signal impending problems. We previously found atherosclerosis iliohypogastric arteries in rabbit ED, down-regulates cavernosal neuronal nitric oxide synthase (nNOS) gene expression, and impairs NO synthesis. The goal this study was determine effect atherosclerosis-induced ischemia on nNOS, endothelial NOS (eNOS), inducible (iNOS) expression NO-mediated smooth muscle relaxation rabbit. Our showed iliac artery blood flow, intracavernosal oxygen tension were unchanged 4 weeks after induction arterial atherosclerosis, whereas they significantly diminished at 8 16. Erectile responses nerve stimulation week 16 atherosclerosis. Western blotting nNOS eNOS protein levels unaffected but decreased iNOS protein, however, markedly increased during course induced disease. Immunohistochemical staining no change or 4. A dramatic decrease both evident weeks. progressively between Down-regulation eNOS, along up-regulation iNOS, may explain ischemic impairment Ischemically altered great pathophysiologic importance These data provide further insight into mechanism arteriogenic dysfunction, oxyoen tension.