Purpose: Acetazolamide and CO2 are cerebral vasodilators whose specifi
c effects in various brain regions have not been carefully defined. We
investigated the effects of these agents in both larger cerebral and
smaller, retrobulbar arteries, to compare their general cerebral vasod
ilatory influence with their specific ocular vascular effects. Methods
: Twelve young adults with healthy eyes were studied under normocapnic
and hypercapnic (6% CO2, 94% O-2 tanked gas) conditions after receivi
ng either placebo or 1,000 mg acetazolamide (3 h before study). Color
Doppler imaging was used to measure peak systolic and end-diastolic ve
locities (PSV and EDV) in the internal carotid, middle cerebral, ophth
almic, and central retinal arteries under each condition. Results: Ace
tazolamide and CO2 each lowered intraocular pressure; combining the ag
ents provided no additive ocular hypotensive effect. Hypercapnia or ac
etazolamide per se failed to alter PSV, EDV, or the derived resistance
index [RI; (PSV - EDV)/PSV] in the internal carotid or in either orbi
tal artery. However, when hypercapnia was superimposed upon acetazolam
ide, the resistance index fell in the internal carotid and central ret
inal arteries (each p < 0.05). In contrast, the middle cerebral artery
was responsive to either vasodilator and to their combination: PSV an
d EDV rose, and RI fell with each experimental treatment. Conclusions:
In the brain, the middle cerebral artery exhibits substantial depende
nce of flow velocity on the vasodilators CO2 and acetazolamide, In con
trast, the ophthalmic and central retinal arteries appear less respons
ive. Nonetheless, the combination of carbonic anhydrase inhibition (ac
etazolamide) with CO2 augmentation did lower vascular resistance dista
l to the central retinal artery, suggesting that this mechanism vasodi
lates critical ocular tissues.