Purpose: Acute oral water loading transiently elevates intraocular pressure
(IOP) via mechanisms that remain unexplained. We tested the possibilities
that water drinking might elevate IOP by creating a blood-aqueous osmotic g
radient, or that it might instead alter active ion pumping and the formatio
n of aqueous humor.
Methods: In the first series, 16 young, healthy individuals were studied du
ring dehydration and for 1 hour after rehydration (14 mL H2O/kg body weight
). Hematocrit, total plasma osmolality, and plasma colloid osmotic pressure
were determined simultaneously with measurements of IOP. In a second serie
s (N = 16), rehydration occurred after pretreatment with either placebo or
a topical carbonic anhydrase inhibitor (1 drop 2% dorzolamide in each eye,
12 and 2 hours before oral water loading).
Results: In both series, mean IOP increased significantly 15 minutes after
water ingestion and remained elevated above baseline for 45 minutes. In con
trast, colloid osmotic pressure and hematocrit were unaltered by water drin
king, and neither these variables nor total plasma osmolality correlated wi
th IOP. In the second series, pretreatment with dorzolamide reduced baselin
e IOP, but failed to alter the magnitude or time course of IOP elevations i
nduced by water drinking.
Conclusion: Because water drinking failed to create a blood-ocular osmotic
pressure gradient, neither vitreous hydration nor increased aqueous ultrafi
ltration can explain increases in IOP after acute hydration. Because the in
crease in ocular tension apparently also is independent of active bicarbona
te pumping, factors affecting aqueous drainage must explain the water drink
ing effect.