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Br J Ophthalmol 2004;88:406-411 doi:10.1136/bjo.2002.008995
  • Clinical science
    • Extended reports

Ocular haemodynamic responses to induced hypercapnia and hyperoxia in glaucoma

  1. S L Hosking1,
  2. A Harris2,
  3. H S Chung2,
  4. C P Jonescu-Cuypers2,
  5. L Kagemann2,
  6. E J Roff Hilton1,
  7. H Garzozi2
  1. 1Neurosciences Research Institute, School of Life and Health Sciences, Aston University, Aston Triangle, Birmingham B4 7ET, UK
  2. 2Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, IN, USA
  1. Correspondence to: A Harris Professor of ophthalmology, physiology and biophysics, Indiana School of Medicine, 702 Rotary Circle, Indianapolis, IN 46202, USA; alharrislear.ucs.indiana.edu
  • Accepted 16 February 2003

Abstract

Aim: To determine the ocular haemodynamic response to gas perturbations in glaucoma.

Methods: 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 PCO2 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.

Results: 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).

Conclusions: These findings suggest the presence of relative vasoconstriction in glaucoma patients, which is at least partially reversed by hypercapnia.

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