Glaucoma and Retina Research Group, Department of Ophthalmology and Vision Sciences, University of Toronto, Toronto, Ontario, Canada.
Invest Ophthalmol Vis Sci. 2010 Apr;51(4):2043-50. doi: 10.1167/iovs.09-3630. Epub 2009 Nov 11.
Purpose. To determine (1) the magnitude of retinal arteriolar vascular reactivity to normoxic hypercapnia in patients with untreated primary open-angle glaucoma (uPOAG) or progressive (p)POAG and in control subjects and (2) the effect of treatment with 2% dorzolamide on retinal vascular reactivity in uPOAG. Methods. The sample comprised 11 patients with uPOAG (after undergoing treatment, they became treated (t)POAG), 17 patients with pPOAG (i.e., manifesting optic disc hemorrhage), and 17 age-similar control subjects. The partial pressure of end-tidal CO(2) (PetCO(2)) was stabilized at 38 mm Hg at baseline. After baseline (10 minutes), normoxic hypercapnia was then induced (15 minutes) with an automated gas flow controller. Retinal arteriolar and optic nerve head (ONH) blood hemodynamics were assessed. The procedures were repeated after treatment with 2% dorzolamide for 2 weeks in tPOAG. Results. Baseline arteriolar hemodynamics were not different across the groups. In control subjects, diameter, velocity, and flow increased (P < 0.001) in response to normoxic hypercapnia. There was no change in all three hemodynamic parameters to normoxic hypercapnia in uPOAG, whereas only blood flow increased (P = 0.030) in pPOAG. Vascular reactivity was decreased in uPOAG and pPOAG patients compared with that in control subjects. After treatment with topical 2% dorzolamide for 2 weeks, the tPOAG group showed an increase in diameter, velocity, and flow (P </= 0.04) in response to normoxic hypercapnia. Similar trends were noted for ONH vascular reactivity. Conclusions. A reduced magnitude of arteriolar vascular reactivity in response to normoxic hypercapnia was shown in uPOAG and in pPOAG. Vascular reactivity improved after dorzolamide treatment in POAG.
目的。确定（1）未经治疗的原发性开角型青光眼（uPOAG）或进展性（p）POAG 患者以及对照组患者对吸氧高碳酸血症的视网膜小动脉血管反应性的程度，以及（2）用 2%多佐胺治疗对 uPOAG 视网膜血管反应性的影响。方法。样本包括 11 例 uPOAG 患者（经治疗后成为治疗（t）POAG）、17 例 pPOAG 患者（即出现视盘出血）和 17 例年龄相似的对照组患者。在基线时将呼气末二氧化碳分压（PetCO2）稳定在 38mmHg。在基线（10 分钟）后，用自动气体流量控制器诱导吸氧高碳酸血症（15 分钟）。评估视网膜小动脉和视神经头（ONH）的血液动力学。在 tPOAG 中用 2%多佐胺治疗 2 周后重复这些程序。结果。各组的基线小动脉血流动力学无差异。在对照组中，直径、速度和流量均增加（P<0.001），以应对吸氧高碳酸血症。uPOAG 对吸氧高碳酸血症无任何血流动力学参数改变，而 pPOAG 只有血流增加（P=0.030）。uPOAG 和 pPOAG 患者的血管反应性较对照组降低。用局部 2%多佐胺治疗 2 周后，tPOAG 组对吸氧高碳酸血症的直径、速度和流量增加（P≤0.04）。ONH 血管反应性也有类似的趋势。结论。uPOAG 和 pPOAG 患者对吸氧高碳酸血症的小动脉血管反应性降低。多佐胺治疗后 POAG 的血管反应性改善。
