*Glaucoma Service, Department of Ophthalmology, School of Medicine daggerSchool of Optometry double dagger;Department of Physiology and Biophysics, Indiana University, Indianapolis, Indiana, U.S.A.
J Glaucoma. 1994 Fall;3(3):226-31.
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.
严重的、短期的肺泡 Pco2 降低会使眼内压（IOP）急性降低。我们想知道，不那么严重的、生理相关的 Pco2 降低是否也会降低眼内压，以及这种效应是否会持续更长时间。为了研究小的 Pco2 变化对 IOP 的急性影响，我们让 11 名健康人通过先将呼气末 Pco2 降低 10%（5 分钟），然后降低 20%（5 分钟）来进行过度通气。当 Pco2 降低 20%时，IOP 下降（14.5 +/- 2.1 mmHg 与匹配的对照组相比，16.8 +/- 1.0 mmHg；p < 0.05），并且在 Pco2 恢复到基线水平后 20 分钟仍保持降低状态。为了研究这种低碳酸血症相关的 IOP 降低随时间的持续时间，我们让 9 名健康人通过过度通气将呼气末 Pco2 降低 15%持续 1 小时。IOP 在 30 分钟时明显降低（11.7 +/- 0.5 与 14.8 +/- 0.6 mmHg 相比；p < 0.05），在 60 分钟时（11.2 +/- 0.7 与 14.2 +/- 0.6 mmHg 相比；p < 0.05）持续低碳酸血症时。相比之下，当比较急性低碳酸血症的效果与标准非选择性β-肾上腺素能阻滞剂（左布诺洛尔 HC1，在研究前 12 小时和 2 小时各滴入 1 滴 0.5%溶液；N = 7 名正常人）时，20%的 Pco2 降低降低 IOP 的效果不如药物治疗，并且在药物治疗后，诱导低碳酸血症未能改变 IOP[基础 IOP 为 14.4 +/- 1.3 mmHg 与左布诺洛尔后 10.0 +/- 1.6 mmHg 相比（p < 0.05），并且在低碳酸血症和左布诺洛尔联合治疗后为 10.7 +/- 1.9 mmHg]。此外，3 天的通气刺激药物甲羟孕酮（每天 150 mg，在 10 名男性中，初始 IOP <= 18 mmHg）治疗显著提高了通气并降低了 Pco2，但未能改变 IOP。我们的结论是，尽管 IOP 与 Pco2 在短期内明显相关，但单独或与药物治疗联合，对 Pco2 的操纵可能不是长期降低 IOP 的有效手段。
