292 EFFECT OF MELATONIN ON CHRONIC BLADDER ISCHEMIA ASSOCIATED CHANGES IN RAT BLADDER FUNCTION

Abstract

You have accessJournal of UrologyBladder and Urethra: Anatomy, Physiology and Pharmacology (I)1 Apr 2013292 EFFECT OF MELATONIN ON CHRONIC BLADDER ISCHEMIA ASSOCIATED CHANGES IN RAT BLADDER FUNCTION Masanori Nomiya, Norifumi Sawada, Mona Zarifpour, Osamu Yamaguchi, and Karl-Erik Andersson Masanori NomiyaMasanori Nomiya Fukushima, Japan More articles by this author , Norifumi SawadaNorifumi Sawada Winston Salem, NC More articles by this author , Mona ZarifpourMona Zarifpour Winston Salem, NC More articles by this author , Osamu YamaguchiOsamu Yamaguchi Koriyama, Japan More articles by this author , and Karl-Erik AnderssonKarl-Erik Andersson Winston Salem, NC More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.1676AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Arterial occlusive disease (atherosclerosis) and chronic ischemia-related oxidative stress may cause bladder dysfunction, including detrusor overactivity. Melatonin, the major secretory product of the pineal gland, has potent endogenous free radical scavenging and antioxidative properties and protects against oxidative insults. Thus, we investigated the potential therapeutic benefit of melatonin in chronic ischemia-related bladder dysfunction. METHODS Adult male Sprague-Dawley rats were divided into control, arterial injury (AI) and AI with melatonin treatment low (AI-ML)/high dose (AI-MH) groups. AI, AI-ML and AI-MH groups underwent endothelial injury of the iliac arteries and received a 2% cholesterol diet following AI. AI-ML and AI-MH rats were treated with melatonin 2.5 or 20mg/kg/day orally for 8 weeks after AI. The control group received a regular diet. After 8 weeks, urodynamic investigation was performed. Bladder tissues and iliac arteries were processed for pharmacological studies, immunohistochemical, and histological examination. RESULTS Iliac arteries from AI, AI-ML and AI-MH rats displayed neo-intimal formation and luminal occlusion. In the AI group, micturition interval was significantly shorter, and bladder capacity and voided volume lower than in the controls. Contractile responses of bladder strips to KCL, electrical field stimulation and carbachol were significantly lower after AI than in the controls. The AI bladders showed significantly increased collagen ratio, oxidative stress and iNOS expression, and decreased constitutive NOS expression compared with the controls. In the AI-ML and AI-MH groups, neo-intimal formation was not prevented, but there were beneficial effects on bladder function and morphology. In the AI-ML group, the beneficial effects failed to reach statistical significance. However, in the AI-MH group, melatonin significantly improved oxidative stress and NOS expression, and there were significant improvements in all the functional and morphological parameters compared with the AI group. CONCLUSIONS Arterial occlusive disease may lead to chronic bladder ischemia and bladder hyperactivity associated with oxidative stress. In the model used, chronic treatment with melatonin protected bladder function and morphology, probably through its free radical scavenging and antioxidative properties. Melatonin may prevent oxidative damage and improve ischemia-related bladder dysfunction. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e119 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Masanori Nomiya Fukushima, Japan More articles by this author Norifumi Sawada Winston Salem, NC More articles by this author Mona Zarifpour Winston Salem, NC More articles by this author Osamu Yamaguchi Koriyama, Japan More articles by this author Karl-Erik Andersson Winston Salem, NC More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...