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EFFICACY

TABLE 2. Choroidal Perfusion by Indocyanine Green Angiography
Timolol (Control) Timolol Dorzolamide
Baseline Drug Baseline Drug
Mean 10% response time (six regions; seconds) 23.1 1.9 23.9 2.4 24.0 1.3 23.3 1.8
Peripapillary minus perimacular 10% response time (seconds) 2.1 0.4 2.2 0.3 1.6 0.3 2.4 0.7
Mean 63% response time ( ; seconds after 10% response) 10.4 0.7 10.3 0.6 10.2 0.5 9.9 0.5
Mean slope (indocyanine green fluorescence/time) .087 .010 .081 .008 .095 .021 .070 .010
Dye duration (70% peak to 70% peak, seconds) 10.2 1.1 9.7 0.8 9.9 1.2 9.8 0.8
Six peripapillary and perimacular choroidal regions are analyzed.
10% time time from injection to achievement of 10% of maximum brightness; 63% response time ( ) time from injection to
achievement of 63% of maximum brightness; Slope slope of filling curve during dye arrival, measured from 40% to 60%; Dye duration
amount of time that fluorescence exceeds 70% of total, representing passage of the bolus.

TABLE 3. Retrobulbar Hemodynamics by Color Doppler Imaging

Timolol (Control) Timolol Dorzolamide
Baseline Drug Baseline Drug
Ophthalmic artery
Peak systolic velocity (cm/second) 27.4 1.8 28.1 2.2 28.2 2.0 27.7 2.5
End-diastolic velocity (cm/second) 7.3 0.7 7.1 0.7 7.5 0.6 6.7 0.4
Resistance index .738 .014 .749 .016 .734 .011 .751 .018
Central retinal artery
Peak systolic velocity (cm/second) 7.1 0.5 6.8 0.5 6.7 0.7 6.7 0.4
End-diastolic velocity (cm/second) 1.7 0.2 1.5 0.1 1.5 0.1 1.5 0.2
Resistance index .749 .018 .769 .013 .757 .015 .771 .019
Nasal posterior ciliary artery
Peak systolic velocity (cm/second) 6.5 0.5 5.9 0.4 6.3 0.5 6.1 0.4
End-diastolic velocity (cm/second) 1.9 0.3 1.6 0.1 1.6 0.1 1.7 0.1
Resistance index .706 .022 .729 .014 .737 .014 .712 .022
Temporal posterior ciliary artery
Peak systolic velocity (cm/second) 5.9 0.3 5.6 0.3 5.9 0.3 5.8 0.4
End-diastolic velocity (cm/second) 1.7 0.2 1.5 0.1 1.6 0.1 1.7 0.1
Resistance index .711 .022 .724 0.13 .721 .014 .695 .024

ular pressure reduction in the two groups. 12 Another this failure is related to the different patient groups studied
possibility is that topical carbonic anhydrase inhibition could in these experiments, or to the simultaneous presence of
directly relax local resistance vessels; systemic carbonic anhy- timolol. This finding does suggest that despite accelerating
drase inhibition clearly increases both cerebral and retinal retinal arteriovenous passage time, dorzolamide augmenta-
blood flow by means of pressure-independent mecha- tion did not improve macular perfusion, either by enhanc-
nisms. 13,14 However, it remains entirely speculative if the ing perifoveal retinal circulation (which nourishes the
inhibition of carbonic anhydrase II and IV in the anterior eye, retinal ganglion cells near the fovea) or the perimacular
as induced by dorzolamide, impacts vascular tone. 1,15 In fact, choroidal circulation (if photoreceptor dysfunction is in-
the mechanism by which systemic carbonic anhydrase inhi- deed involved in the pathophysiology of glaucoma). 18,19
bition increases cerebral perfusion remains unclear: the role It may appear unusual that application of an eye drop
that ATP-sensitive K channels, nitric oxide, vasodilating would produce a vascular response in the superior retinal
prostanoids, or cAMP or cGMP may play in this response is vasculature alone. The mere existence of hemifield defects
undefined. 16 in glaucoma suggest that the superior and inferior ocular
Unlike previous studies of dorzolamide in healthy per- hemispheres may exhibit independent and differing func-
sons or patients with normal-tension glaucoma, in patients tion. Previously published data on ocular vascular response
with primary open-angle glaucoma we found no effects of to hypercapnea and hyperoxia have been analyzed. 20 The
dorzolamide-timolol combination on contrast sensitivity Heidelberg retina flowmeter, a scanning laser Doppler
or any other aspect of visual function. 5,17 It is unclear if device, found that the inferior retina alone responded to

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