Abstract

You have accessJournal of UrologyUrodynamics/Incontinence/Female Urology: Basic Research (1)1 Apr 201340 SLEEP APNEA CAUSES BLADDER OXIDATIVE STRESS AND NUCTURIA IN RATS Kazem Azadzoi, Farzana Nipa, Yedan Li, and Mike Siroky Kazem AzadzoiKazem Azadzoi Boston, MA More articles by this author , Farzana NipaFarzana Nipa Boston, MA More articles by this author , Yedan LiYedan Li Boston, MA More articles by this author , and Mike SirokyMike Siroky Boston, MA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.1415AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Sleep apnea (SA) is a chronic condition affecting over 18 million adults in the United States where the affected person repeatedly stops breathing during sleep causing blood oxygen levels to drop and then rapidly increase with breathing. This initiates repeating cycles of hypoxia and reoxygenation. The incidence of SA closely correlates with the prevalence of nocturia. Our goal was to assess bladder oxidative stress markers and examine micturition behavior and cystometric parameters in a rat model of SA. METHODS Male Sprague-Dawley rats were divided into treatment (SA, n=8), sham (n=8) and control (n=8) groups. The treatment group was exposed to conditions similar to SA by housing the animals in computerized servo-controlled oxycyclers that produced reductions in ambient oxygen level from 21% to 8% for 8 seconds then rebound to 21% oxygen for 20 seconds. The computer was programed to repeat this cycle every 90 seconds for 8 hours daily for 8 weeks. The sham group was housed under similar oxycycler conditions with air supply alternating slightly from 21% to 20% oxygen 8 hours daily for 8 weeks. The control group was not exposed to oxycycler and used as age-matched control. After 8 weeks, day and night time voiding behavior of animals were assessed in metabolic cages under 12:12 hours light/dark cycles conditions. After this, cystometrograms were obtained then bladder tissues were processed for biochemical assays, ELISA and transmission electron microscopy (TEM). RESULTS Animals exposure to SA conditions significantly increased micturition frequency and diminished voided volume. Cystometrograms showed a significant increase in spontaneous bladder contractions in animals exposed to SA conditions in comparison with sham and control animals. The duration and amplitude of bladder contractions were significantly greater in the SA group. ELISA of bladder samples from SA group showed oxidative tissue damage characterized by increases in protein oxidation and lipid peroxidation products, decrease in antioxidant enzymatic activity, and accumulation of the oxidative product 8-isoprostane PGF2 alpha and nitrosative product nitrotyrosine. TEM of bladder samples from SA group showed swollen mitochondria, loss of mitochondrial cristae, and diffused accumulation of connective tissue. CONCLUSIONS SA exposes the bladder to oxidative stress and may play a role in the development of nocturia. The mechanism appears to involve free radical incursion of the cellular and subcellular elements and oxidative modification of the bladder mitochondrial energy apparatus and smooth muscle contractile component. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e16 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Kazem Azadzoi Boston, MA More articles by this author Farzana Nipa Boston, MA More articles by this author Yedan Li Boston, MA More articles by this author Mike Siroky Boston, MA More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

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