Hosking S L, Harris A, Chung H S, Jonescu-Cuypers C P, Kagemann L, Roff Hilton E J, Garzozi H
Neurosciences Research Institute, School of Life and Health Sciences, Aston University, Aston Triangle, Birmingham B4 7ET, UK.
Br J Ophthalmol. 2004 Mar;88(3):406-11. doi: 10.1136/bjo.2002.008995.
To determine the ocular haemodynamic response to gas perturbations in glaucoma.
Intraocular pressure (IOP), systemic systolic and diastolic blood pressure (SBP and DBP), and retrobulbar blood flow velocities, measured by colour Doppler imaging (CDI), were recorded at two visits. CDI was used to measure peak systolic and end diastolic velocities (PSV and EDV) and resistance index (RI) in the ophthalmic artery (OA), central retinal artery (CRA), and short posterior ciliary arteries (SPCAs). At the first visit, measurements were taken at baseline (B1: breathing room air) and during isoxic hypercapnia (end tidal PCO(2) increased 15% above baseline) in 16 normal subjects and 12 patients with glaucoma. On another day, measurements were repeated at a second baseline (B2) and during hyperoxia (100% oxygen breathing) for 15 normal subjects and 13 glaucoma patients. Baseline systemic data were compared using paired t tests; REANOVA was performed to compare group differences at baseline and to determine the vessel response to each condition. Fisher's LSD was used for post hoc comparison.
Baseline OA PSV was lower for the glaucoma than for the normal group (p = 0.047); the groups were otherwise similar at baseline. IOP demonstrated no response to hypercapnia, but reduced during hyperoxia for both the normal subjects (p<0.0001) and glaucoma patients (p = 0.04). During hypercapnia, SBP increased in normal subjects (p = 0.03) and glaucoma patients (p = 0.01); DBP increased in normal subjects (p = 0.021). There was a corresponding increase in ocular perfusion pressure (OPP) for normal subjects (p = 0.01) and glaucoma subjects (p = 0.028), and as a result OPP was included as a covariate in the REANCOVA model. Hypercapnia resulted in increased PSV in the CRA of normal subjects (p = 0.035) and increased PSV and EDV in the SPCAs of glaucoma patients (p = 0.041 and p = 0.030 respectively). Hyperoxia resulted in reduced PSV and EDV in the ophthalmic arteries of normal subjects only (p = 0.001 and 0.031 respectively).
These findings suggest the presence of relative vasoconstriction in glaucoma patients, which is at least partially reversed by hypercapnia.
确定青光眼患者眼部血流动力学对气体扰动的反应。
在两次就诊时记录眼压(IOP)、体循环收缩压和舒张压(SBP和DBP),以及通过彩色多普勒成像(CDI)测量的球后血流速度。CDI用于测量眼动脉(OA)、视网膜中央动脉(CRA)和睫状后短动脉(SPCA)的收缩期峰值速度和舒张末期速度(PSV和EDV)以及阻力指数(RI)。在首次就诊时,对16名正常受试者和12名青光眼患者在基线(B1:呼吸室内空气)和等氧性高碳酸血症期间(呼气末PCO₂比基线升高15%)进行测量。在另一天,对15名正常受试者和13名青光眼患者在第二个基线(B2)和高氧期间(呼吸100%氧气)重复测量。使用配对t检验比较基线时的体循环数据;进行重复测量方差分析以比较基线时的组间差异,并确定血管对每种情况的反应。采用Fisher最小显著差法进行事后比较。
青光眼患者的基线眼动脉PSV低于正常组(p = 0.047);两组在基线时其他方面相似。眼压对高碳酸血症无反应,但在高氧期间正常受试者(p<0.0001)和青光眼患者(p = 0.04)的眼压均降低。在高碳酸血症期间,正常受试者(p = 0.03)和青光眼患者(p = 0.01)的收缩压升高;正常受试者的舒张压升高(p = 0.021)。正常受试者(p = 0.01)和青光眼受试者(p = 0.028)的眼灌注压(OPP)相应升高,因此在重复测量协方差分析模型中将OPP作为协变量纳入。高碳酸血症导致正常受试者视网膜中央动脉的PSV升高(p = 0.035),青光眼患者睫状后短动脉的PSV和EDV升高(分别为p = 0.041和p = 0.030)。高氧仅导致正常受试者眼动脉的PSV和EDV降低(分别为p = 0.001和p = 0.031)。
这些发现提示青光眼患者存在相对血管收缩,高碳酸血症至少可部分逆转这种情况。