May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
The Effect of Hyperoxia and Hypoxia on the Slow Multifocal Electroretinogram in Diabetic Patients Without Retinopathy
Author Affiliations & Notes
  • K. Klemp
    Ophthalmology, Herlev Hospital, University of Copenhagen, Herlev, Denmark
  • B. Sander
    Ophthalmology, Herlev Hospital, University of Copenhagen, Herlev, Denmark
  • D. Nellemann
    Ophthalmology, Herlev Hospital, University of Copenhagen, Herlev, Denmark
  • M. Larsen
    Ophthalmology, Herlev Hospital, University of Copenhagen, Herlev, Denmark
  • Footnotes
    Commercial Relationships  K. Klemp, None; B. Sander, None; D. Nellemann, None; M. Larsen, None.
  • Footnotes
    Support  The Danish Eye Research Foundation
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 436. doi:
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      K. Klemp, B. Sander, D. Nellemann, M. Larsen; The Effect of Hyperoxia and Hypoxia on the Slow Multifocal Electroretinogram in Diabetic Patients Without Retinopathy . Invest. Ophthalmol. Vis. Sci. 2005;46(13):436.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To compare the effect of hypoxia and hyperoxia on the multifocal electroretinogram (mfERG) in patients with type 1 diabetes without retinopathy and in healthy subjects. Methods: MfERG was recorded in one eye in 8 eyes of 8 diabetic patients and 10 eyes of 10 non–diabetic subjects at three levels of oxygenation: hypoxia induced by 10% oxygen and 90% nitrogen breathing, hyperoxia induced by 100% oxygen breathing and normoxia induced by atmospheric air breathing. MfERGs were recorded using the Veris 5 system. An array of 61 hexagons was displayed at a frame rate of 75 Hz and 3 dark frames were inserted between each m–sequence step. Results:In diabetic patients hyperoxia significantly increased mfERG amplitudes in the central retina (0–2 degrees of eccentricity) by 15.1% (p = 0.008). In healthy subjects, hyperoxia induced no change in mfERG amplitude (0.9%, p > 0.05). Both in diabetic and healthy subjects hyperoxia tended to increase mfERG amplitudes at higher eccentricities to roughly the same magnitude (p > 0.05) and hyperoxia induced no significant changes in mfOP amplitudes. In diabetic patients without retinopathy hypoxia tended to reduced mfERG amplitudes in the central retina (0–2 degrees) by 15.2% (p > 0.05) and in the more peripheral retina by 12.5 – 19.4 % (p > 0.05). In non–diabetic controls, hypoxia reduced central mfERG amplitudes by 38.5% (p < 0.0001) and peripheral amplitudes by 17.8 – 26.8% (p < 0.01). In diabetic patients hypoxia decreased the summed mean OP1 and OP2 amplitudes by 18.6 (p = 0.03) and 22.5% (p = 0.001), respectively. In healthy subjects hypoxia decreased the summed mean OP1 and OP2 amplitudes by 26.7 (p < 0.0001) and 26.8% (p < 0.0001), respectively. In both diabetic patients and healthy controls mfERG implicit times were unaffected by changes in arterial oxygen tension. Transcutaneous monitoring of peripheral blood oxygenation demonstrated quantitatively comparable changes in diabetic and healthy subjects. In diabetic subjects, mean blood saturation during hypoxic recordings (73.3%) slightly exceeded that of healthy subjects (69.4%). Conclusions: Our results indicate that diabetes without diabetic retinopathy is associated with significant changes in retinal metabolism, as assessed by the ability of the retina to produce electroretinographic potentials. In conjunction with previous studies of the role of glucose, these results indicate a crucial role for changes in substrate supply and utilization in the retina during hyperglycemia with potential implications for the development of diabetic microangiopathy in the retina.

Keywords: diabetes • hypoxia • electroretinography: clinical 
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