706 CEREBRAL HEMODYNAMIC RESPONSES TO SILDENAFIL IN HEALTHY MALE'S VOLUNTEERS

Abstract

You have accessJournal of UrologySexual Function/Dysfunction/Andrology: Basic Research I1 Apr 2010706 CEREBRAL HEMODYNAMIC RESPONSES TO SILDENAFIL IN HEALTHY MALE'S VOLUNTEERS Yoram Vardi, Shadi Jahshan, Muhannad Massoud, Ilan Gruenwald, Menashe Zaaroor, and Giris Jacob Yoram VardiYoram Vardi More articles by this author , Shadi JahshanShadi Jahshan More articles by this author , Muhannad MassoudMuhannad Massoud More articles by this author , Ilan GruenwaldIlan Gruenwald More articles by this author , Menashe ZaaroorMenashe Zaaroor More articles by this author , and Giris JacobGiris Jacob More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2010.02.1147AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES The most prevalent side effect of sildenafil is headache, yet the mechanism that causes this symptom is unknown. In this study we aimed to test the hypothesis that sildenafil-induced headache may be caused by its effect on cerebrovascular autoregulation (CVAR). METHODS Fourteen young healthy males, 34±2 years old, were enrolled in the study. Beat-to-beat Bp and ECG, cerebral blood flow velocity (CBFv) measured with TCD, and end tidal CO2 (EtCO2) were assessed at baseline (EtCO2 ∼ 40), during hyperventilation (EtCO2 ∼ 24), hypercapnia (EtCO2 ∼ 48), during graded tilt and at graded doses of I.V. phenylephrine (25-200 ugs). The study was repeated one hour after oral sildenafil 100 mg. CO2-vasoreactivity was extrapolated from the changes in CO2 the correspondent changes in mean CBFv. Both pressure dependent CVAR mechanisms, static and dynamic, were assessed by plotting the changes in CBFv against the changes in BP during the graded tilt and the phenylephrine responses, respectively. RESULTS Rest supine BP, HR, peak and mean CBFv, respiratory rate and EtCO2 were 117±2/67±3 mm Hg, 69±3 bpm, 84±6 and 57±4 cm/sec, 16±0.5 resp/min and 39±0.9 mm Hg, respectively. These parameters were not affected by sildenafil except for an increase in HR by 4.5±2 bpm (p=0.03). Sildenafil caused significant increase in the CO2-vasoreactivity index, from 1.62±0.1 to 1.83±0.15 cm/sec * mm Hg (p=0.04). However, acute PDE5 inhibition did not cause any change in the cerebrovascular hemodynamic responses to tilt and graded doses of phenylephrine. CONCLUSIONS Sildenafil enhances the cerebrovascular CO2-reactivity without affecting the pressure dependent autoregulatory mechanisms. This effect is probably mediated by the interference of the PDE5I in the nitric oxide pathway. Data are needed to test this effect in pathological stated. This new mechanism of action may have some therapeutically implications. Haifa, Israel© 2010 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 183Issue 4SApril 2010Page: e275-e276 Advertisement Copyright & Permissions© 2010 by American Urological Association Education and Research, Inc.MetricsAuthor Information Yoram Vardi More articles by this author Shadi Jahshan More articles by this author Muhannad Massoud More articles by this author Ilan Gruenwald More articles by this author Menashe Zaaroor More articles by this author Giris Jacob More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...