Abstract
Purpose :
Bursts of sympathetic activity, seen in pathologies like sleep apnea, may lead to increased local vascular resistance (VR) in ocular vasculature, potentially reducing ocular perfusion and increasing the risk of ischemic damage to the eye. We performed a prospective repeated-measures study to explore our hypotheses that a) sympathetic activity increases VR in vessels supplying the optic nerve head (ONH), choroid, and retina; and b) the commonly used ophthalmic medications brimonidine, an α2 agonist, and dorzolamide, a carbonic anhydrase inhibitor, could prevent increases in VR.
Methods :
Ten healthy subjects (age 50-80) pretreated one eye with 1 drop of brimonidine TID for 3 days, then had their intraocular pressures measured with a Tono-Pen and measurements of peripheral arterial tone (PAT) amplitude, a measure inversely related to sympathetic activity, collected using WatchPAT 300 devices on both index fingers. Ocular blood flow (via laser speckle flowgraphy) and blood pressures were recorded at baseline and after submerging one foot in an ice-water bath (IWB) for 2 minutes. Patients repeated this protocol following a one-week washout and pretreating the same eye with 1 drop of dorzolamide (20 mg/mL) TID for 3 days. One-tailed paired t-tests were used for statistical analyses.
Results :
Peripheral sympathetic activity was significantly increased following the IWB (p<0.0001). Increases in VR with the IWB were found in the ONH (p=0.0076), retina (p=0.0331), and choroid (p=0.0277) in untreated fellow eyes in dorzolamide trials. Pre-treatment with dorzolamide prevented an increase in VR in retinal vessels (p=0.3157) but significant VR increases still occurred in the ONH (p=0.0196) and choroid (p=0.0196). Pre-treatment with brimonidine did not prevent an increase in VR produced in the ONH (p=0.0195).
Conclusions :
An increase in sympathetic activity was associated with increased VR in each vascular bed in dorzolamide trials. These effects were attenuated in the retinal vessels by topical dorzolamide. The lack of effect of dorzolamide on the choroid and ONH and lack of effect of brimonidine on all ocular vascular beds may be due to inadequate drug delivery to these vascular beds with topical administration. Future experiments in patients with unilateral Horner’s syndrome may further elucidate the role of sympathetic innervation on modulation of ocular perfusion.
This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.