TY - JOUR
T1 - The effect of systemic hyperoxia on optic nerve head blood flow in primary open-angle glaucoma patients
AU - Kiyota, Naoki
AU - Shiga, Yukihiro
AU - Suzuki, Shiori
AU - Sato, Marika
AU - Takada, Naoko
AU - Maekawa, Shigeto
AU - Omodaka, Kazuko
AU - Maruyama, Kazuichi
AU - Kunikata, Hiroshi
AU - Nakazawa, Toru
N1 - Funding Information:
Supported in part by the JSPS KAKENHI Grants-in-Aid for Scientific Research (B) (TN 26293372), for Exploratory Research (TN 26670751), and by JST Center for Revitalization Promotion
Publisher Copyright:
© 2017 The Authors.
PY - 2017/6
Y1 - 2017/6
N2 - PURPOSE. To assess the optic nerve head blood flow (ONH BF) response to hyperoxia in glaucoma patients using laser speckle flowgraphy (LSFG), and determine factors influencing vasoreactivity within the ONH. METHODS. We performed oxygen provocation testing in 15 eyes of 15 primary open-angle glaucoma (POAG) patients and 15 eyes of 15 age-matched control subjects. During the test, LSFG-derived tissue mean blur rate (MBRT) and clinical variables, including blood pressure, were recorded. We evaluated differences in MBRT alteration during systemic hyperoxia between the groups. Additionally, we calculated the mean % change in MBRT against baseline and determined contributing factors. RESULTS. Despite similar clinical variables during systemic hyperoxia in both groups, the mean % change in MBRT against baseline was significantly lower in the POAG than control subjects (P < 0.0001). Multiple regression analysis revealed that baseline MBRT and systolic blood pressure (SBP) were contributing factors to mean % change in MBRT (β = 0.44, β = –0.32, respectively). Additionally, baseline MBRT and SBP were strongly correlated to mean % change in MBRT only in the POAG group (r = 0.83, P < 0.0001; r = –0.60, P = 0.02, respectively). CONCLUSIONS. POAG patients had a weaker vasoreactive response to hyperoxia than controls, and this impaired response was associated with lower basal ONH BF and higher SBP. These findings suggest that pre-existing vasoconstriction in the ONH of eyes with glaucoma might reduce the capacity of the vasoconstrictive response to hyperoxia. Alternatively, the pathways that mediate hyperoxia-induced vasoconstriction could be altered in POAG.
AB - PURPOSE. To assess the optic nerve head blood flow (ONH BF) response to hyperoxia in glaucoma patients using laser speckle flowgraphy (LSFG), and determine factors influencing vasoreactivity within the ONH. METHODS. We performed oxygen provocation testing in 15 eyes of 15 primary open-angle glaucoma (POAG) patients and 15 eyes of 15 age-matched control subjects. During the test, LSFG-derived tissue mean blur rate (MBRT) and clinical variables, including blood pressure, were recorded. We evaluated differences in MBRT alteration during systemic hyperoxia between the groups. Additionally, we calculated the mean % change in MBRT against baseline and determined contributing factors. RESULTS. Despite similar clinical variables during systemic hyperoxia in both groups, the mean % change in MBRT against baseline was significantly lower in the POAG than control subjects (P < 0.0001). Multiple regression analysis revealed that baseline MBRT and systolic blood pressure (SBP) were contributing factors to mean % change in MBRT (β = 0.44, β = –0.32, respectively). Additionally, baseline MBRT and SBP were strongly correlated to mean % change in MBRT only in the POAG group (r = 0.83, P < 0.0001; r = –0.60, P = 0.02, respectively). CONCLUSIONS. POAG patients had a weaker vasoreactive response to hyperoxia than controls, and this impaired response was associated with lower basal ONH BF and higher SBP. These findings suggest that pre-existing vasoconstriction in the ONH of eyes with glaucoma might reduce the capacity of the vasoconstrictive response to hyperoxia. Alternatively, the pathways that mediate hyperoxia-induced vasoconstriction could be altered in POAG.
KW - Autoregulation
KW - Hyperoxia
KW - Laser speckle flowgraphy
KW - Ocular blood flow
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U2 - 10.1167/iovs.17-21648
DO - 10.1167/iovs.17-21648
M3 - Article
C2 - 28654983
AN - SCOPUS:85021911561
SN - 0146-0404
VL - 58
SP - 3181
EP - 3188
JO - Investigative Ophthalmology
JF - Investigative Ophthalmology
IS - 7
ER -