PURPOSE. To determine whether corneal acidosis, which occurs during contact
lens wear, alters corneal O-2 consumption (QO(2)) and if so, whether incre
ased ion transport activity could contribute to altered QO(2) during acidos
is.
METHODS. PO2 was measured, using the phosphorescence quenching of Pd-meso-t
etra-(4-carboxyphenyl) porphine, in an airtight chamber that held a trephin
ed rabbit cornea. The rate of change in chamber PO2 was used as a measure o
f QO(2). QO(2) was measured at pH 7.5 and then at either pH 6.7, 7.1, or 7.
3 Measurements of QO(2) at pHs 7.5 and 6.7 were repeated in the presence of
0.5 mM amiloride and 0.5 mM ouabain.
RESULTS. When pH was changed from 7.5 to 6.7, 7.1, or 7.3, O-2 consumption
increased by a factor of 1.80 +/- 0.11 (+/-SF), 1.65 +/- 0.12, and 1.44 +/-
0.06, respectively. Amiloride (0.5 mM) and ouabain (0.5 mM) inhibited 50%
and 65%, respectively, of the increase in QO(2) at pH 6.7.
CONCLUSIONS. Corneal acidosis leads to increased QO(2) in a dose-dependent
manner. The increased QO(2) is in part secondary to the activation of pH re
gulatory mechanisms, including Na+/H+ exchange, which then stimulates Na+/K
+-ATPase activity. These findings indicate that contact lens-induced acidos
is can exacerbate corneal hypoxia and related complications.