Ocular hypotension during short- and long-term hypocapnia.

Severe, short-term decreases in alveolar Pco2 acutely lower intraocular pressure (IOP). We wondered if less severe, physiologically relevant Pco2 reductions would also lower ocular tension and if this effect would persist in the longer term. To investigate the acute influence of small Pco2 changes on IOP, 11 healthy persons hyperventilated to reduce end-tidal Pco2 by first 10% (5 min) and then 20% (5 min). IOP fell when Pco2 fell 20% (14.5 +/- 2.1 mm Hg vs, 16.8 +/- 1.0 in a matched control series; p < 0.05) and remained depressed 20 min after Pco2 had returned to baseline levels. To investigate the persistence over time of this hypocapnia-associated IOP reduction, nine healthy persons hyperventilated to reduce end-tidal Pco2 by 15% for 1 h. IOP was substantially reduced by 30 min (11.7 +/- 0.5 vs. 14.8 +/- 0.6 mm Hg; p < 0.05) and at 60 min (11.2 +/- 0.7 vs. 14.2 +/- 0.6 mm Hg; p < 0.05) of sustained hypocapnia. In contrast, when the effects of acute hypocapnia were compared with standard nonselective beta-adrenergic blockade (levobunolol HC1, 1 drop 0.5% solution instilled 12 and 2 h before study; N = 7 normals), a 20% Pco2 reduction was less effective in lowering IOP than was drug treatment, and induction of hypocapnia failed to alter IOP after drug treatment [baseline IOP 14.4 +/- 1.3 mm Hg vs. 10.0 +/- 1.6 mm Hg after levobunolol (p < 0.05) and 10.7 +/- 1.9 mm Hg after hypocapnia and levobunolol were combined]. In addition, 3 days' treatment with the ventilatory stimulant drug medroxyprogesterone acetate (150 mg/day in 10 men, initial IOP </= 18 mm Hg) significantly elevated ventilation and lowered Pco2 but failed to change IOP. We conclude that although IOP is clearly linked to Pco2 in the short term, manipulation of Pco2, either alone or in combination with drug therapy, may not be an effective means for long-term IOP reduction.