Published ahead of print on June 5, 2008, doi:10.1164/rccm.200801-190OC Am. J. Respir. Crit. Care Med., Volume 178, Number 6, September 2008, 644-650 A more recent version of this article appeared on September 15, 2008
Submitted on January 31, 2008 Erectile Dysfunction In a Murine Model of Sleep ApneaGalia K Soukhova-O'Hare1,1 Department of Pediatrics, Kosair Children's Hospital Research Institute, University of Louisville, Louisville, KY, USA; Department of General Physiology, St. Petersburg State University, St. Petersburg, Russian Federation, 2 Department of Pediatrics, Kosair Children's Hospital Research Institute, University of Louisville, Louisville, KY, USA, 3 Department of Obstetrics and Gynecology, University of Louisville, Louisville, KY, USA, 4 Department of General Physiology, St. Petersburg State University, St. Petersburg, Russian Federation, 5 Department of Pediatrics, Kosair Children's Hospital Research Institute, University of Louisville, Louisville, KY, USA; Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, USA * To whom correspondence should be addressed. E-mail: david.gozal{at}louisville.edu.
Introduction: Erectile dysfunction (ED) is frequent in obstructive sleep apnea syndrome (OSAS). Chronic intermittent hypoxia (CIH), one of the hallmarks of OSAS, could mediate ED. Methods: Three groups of C57BL/6 mice were exposed to CIH for 5 or 24 weeks. Sexual function was evaluated by in vivo telemetry of corpus spongiosum pressure (CSP). Spontaneous erections, sexual activity during mating, and non-contact tests were assessed after 5 wks of CIH and following treatment with tadalafil. Plasma testosterone was measured after 8 and 24 wks of CIH, and the expression of nitric oxide synthase isoforms (NOS) was examined in penile tissue. Results: Non-contact, spontaneous and contact sexual activity in the mice were suppressed after CIH. Spontaneous erection counts decreased following the first week of CIH by 55% (P<0.001) and remained unchanged thereafter. Recovery of erectile activity during normoxia for 6 weeks was incomplete. Compared to control mice, latencies for mounts and intromissions increased by 60 and 40 fold respectively (P<0.001), and the sexual activity index decreased 6-fold. Tadalafil treatment significantly attenuated these effects. Immunoblot analyses of NOS proteins in the erectile tissue showed decreased expression of endothelial NOS after CIH (p<0.01, with no changes in plasma testosterone levels after 8 and 24 weeks of CIH. Conclusions: CIH during sleep is associated with decreased libido in mice. The decreased expression of eNOS protein in erectile tissue and the favorable response to tadalafil suggest that altered nitric oxide mechanisms underlie CIH-mediated ED. No changes in testosterone emerge after IH. Key words: sleep apnea; erectile dysfunction; intermittent hypoxia; testosterone; nitric oxide
This article has been cited by other articles:
|
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
