Harris A, Sergott R C, Spaeth G L, Katz J L, Shoemaker J A, Martin B J
Department of Ophthalmology, Indiana University School of Medicine, Indianapolis 46202.
Am J Ophthalmol. 1994 Nov 15;118(5):642-9. doi: 10.1016/s0002-9394(14)76579-1.
The pathogenesis of normal-tension glaucoma remains unknown. Because ocular vasospasm has been proposed as a possible mechanism, we investigated ocular vessel flow velocity in normal-tension glaucoma patients at rest and under treatment with a cerebral vasodilator. Ten normal-tension glaucoma patients and nine age- and gender-matched controls had flow velocity measured in three vessels (ophthalmic artery, central retinal artery, and temporal short posterior ciliary artery) by using color Doppler imaging, under baseline conditions and during carbon dioxide supplementation sufficient to increase end-tidal PCO2 by 15%. Peak systolic and end-diastolic velocities were measured, and the resistance index (peak systolic velocity minus end-diastolic velocity, divided by peak systolic velocity) was calculated. Compared with controls, these normal-tension glaucoma patients had significantly lower end-diastolic velocities (P = .002) and higher resistance indices (P = .007) in the ophthalmic artery at baseline. When PCO2 was increased, control subjects remained unchanged, whereas it increased end-diastolic velocity in patients (P = .003) and abolished the difference in resistance index between the two groups. Patients and control subjects differed little in their baseline or carbon dioxide response velocities or in resistance in the other two vessels. These results indicate that at baseline these normal-tension glaucoma patients may have increased vascular resistance distal to the ophthalmic artery, although this increased resistance cannot be specifically ascribed to the central retinal arterial or to temporal short posterior ciliary arterial vascular beds. The responsiveness of these patients to a cerebral vasodilator (increased PCO2) indicates further that the increased resistance distal to the ophthalmic artery may be the reversible result of vasospasm.
正常眼压性青光眼的发病机制尚不清楚。由于眼部血管痉挛被认为是一种可能的机制，我们研究了正常眼压性青光眼患者在静息状态下以及使用脑血管扩张剂治疗时的眼部血管流速。10名正常眼压性青光眼患者和9名年龄及性别匹配的对照者，通过彩色多普勒成像在三种血管（眼动脉、视网膜中央动脉和颞侧睫状后短动脉）中测量流速，测量在基线条件下以及补充二氧化碳使呼气末PCO₂增加15%期间进行。测量收缩期峰值流速和舒张末期流速，并计算阻力指数（收缩期峰值流速减去舒张末期流速，再除以收缩期峰值流速）。与对照组相比，这些正常眼压性青光眼患者在基线时眼动脉的舒张末期流速显著降低（P = 0.002），阻力指数更高（P = 0.007）。当PCO₂增加时，对照组受试者没有变化，而患者的舒张末期流速增加（P = 0.003），两组之间阻力指数的差异消失。患者和对照组受试者在基线或二氧化碳反应流速方面，以及在其他两种血管的阻力方面差异不大。这些结果表明，在基线时，这些正常眼压性青光眼患者眼动脉远端的血管阻力可能增加，尽管这种增加的阻力不能具体归因于视网膜中央动脉或颞侧睫状后短动脉血管床。这些患者对脑血管扩张剂（增加PCO₂）的反应进一步表明，眼动脉远端增加的阻力可能是血管痉挛的可逆结果。
