The effect of sildenafil on retinal blood velocity in healthy subjects

Asaf Achiron,Chen Juza,Adiel Barak,Zvia Burgansky-Eliash,Idan Hecht

doi:10.1186/s40662-018-0125-y

Asaf Achiron, Chen Juza + Show 3 more

Open Access

https://doi.org/10.1186/s40662-018-0125-y

Copy DOI

Abstract

PurposeIt has been suggested that Sildenafil may have beneficial therapeutic effects in the treatment of neurodegenerative disorders. The retinal circulation is of significant interest as a marker of cerebral vascular disease since the retinal and cerebral vasculatures share many morphological and physiological properties, yet only the retinal circulation can be directly visualized. Therefore, our aim was to assess the change induced by Sildenafil on retinal blood velocity.MethodsRetinal flow velocity was measured 0.5, 3 and 6 h following administration of 100 mg of Sildenafil using the Retinal Function Imager.ResultsNo clinical change in either systemic blood pressure or retinal flow velocities were observed. However, when controlling for heart rate and blood pressure, a significant drop in venous flow velocity 6 h following treatment (mean drop 0.3 ± 0.07; 95% CI: 0.44–0.56, P = 0.023) was revealed.ConclusionsIn healthy volunteers, retinal venous flow velocity was significantly reduced at the 6-h time point following Sildenafil treatment. No effect was observed on arterial retinal flow velocity.

Highlights

Sildenafil is a selective inhibitor of the intracellular enzyme phosphodiesterase-5 (PDE5) and is widely used as treatment for erectile dysfunction
It has been suggested that Sildenafil may have beneficial therapeutic effects in the treatment of stroke, subarachnoid hemorrhage, dementia, and neurodegenerative disorders by enhancing angiogenesis [5]
No difference was found between arterial velocities across all time points (F = 0.84, P = 0.77).When evaluating flow velocity dependence on selected residual covariance structure, the mixed model showed that heart rate (HR) and mean arterial pressure (MAP) only affect the venous flow (venous: (HR: F = 1939, P < 0.001, MAP: F = 10,753, P < 0.001), arterial: (HR: F = 0.554, P nonsignificant, MAP: F = 0.672, P non-significant))

Summary

Introduction

Sildenafil is a selective inhibitor of the intracellular enzyme phosphodiesterase-5 (PDE5) and is widely used as treatment for erectile dysfunction. Inhibition of cyclic guanosine monophosphate (cGMP)-specific PDE5 results in increased levels of cGMP and nitric oxide. This leads to reduced intracellular calcium levels thereby producing smooth muscle relaxation and an increase in blood flow in erectile tissue [1]. It has been suggested that Sildenafil may have beneficial therapeutic effects in the treatment of stroke, subarachnoid hemorrhage, dementia, and neurodegenerative disorders by enhancing angiogenesis [5]. Several reports have associated Sildenafil with various neurological adverse outcomes.

Objectives

Methods

Results

Conclusion