British Journal of Ophthalmology · 2007 · 18 citations · 28 references
MedicineOphthalmologyPharmacologyCardiovascular PharmacotherapyClinical OptometryOcular PharmacologyIntraocular Pressure MeasurementMedication Effects On VisionOcular PharmacodynamicsBlood FlowChoroidal Blood Flow AssessmentChoroidal MicrovasculatureIntraocular Pressure ReductionLaser Doppler ImagingLaser Doppler VelocimetryRetinal Blood Flow AlterationsRetinal Vessel Analysis
AIM: To evaluate the effect of intravenously administered clonidine on ocular blood flow in healthy volunteers. METHODS: A randomised, double-masked, placebo-controlled, two-way crossover study was performed in 12 healthy young volunteers. Clonidine (0.2 microg/kg/min) or placebo was administered intravenously over 10 minutes. The effects of clonidine were studied at baseline and up to 150 minutes after infusion. Ocular haemodynamics were measured using laser Doppler flowmetry, laser Doppler velocimetry and a retinal vessel analyser. RESULTS: Clonidine significantly decreased mean arterial pressure (MAP) and intraocular pressure (IOP). Calculated ocular perfusion pressure decreased significantly by -8.7+/-8.7% after infusion of clonidine (p<0.01 vs placebo). Retinal arterial diameters increased by +4.4+/-2.7% (p = 0.012 vs placebo), whereas no significant change was observed in retinal veins. Red blood cell velocity decreased by -16+/-14% (p<0.01 vs placebo) after infusion of clonidine. Hence, calculated retinal blood flow decreased by -14+/-12% (p = 0.033 vs placebo). Choroidal blood flow increased by +18+/-19% (p<0.01 vs placebo) and optic nerve head blood flow increased by +16+/-23% (p = 0.046 vs placebo) 30 minutes after administration of clonidine but both returned to baseline thereafter. CONCLUSION: The short-time increase in choroidal and optic nerve head blood flow indicates a transient vasodilatory effect of clonidine due to an unknown mechanism. The decrease in retinal blood flow indicates clonidine-induced vasoconstriction in the retinal microvasculature.
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Central Hypotensive Effects of the α <sub>2a</sub> -Adrenergic Receptor Subtype
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