March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
Evaluation Of Retinal Vasomotor Reactivity During Changes In Arterial Blood Oxygen Content
Author Affiliations & Notes
  • Helene Kergoat
    School of Optometry, University Montreal, Montreal, Quebec, Canada
  • Carl Dutrisac
    School of Optometry, University Montreal, Montreal, Quebec, Canada
  • John V. Lovasik
    School of Optometry, University Montreal, Montreal, Quebec, Canada
  • Footnotes
    Commercial Relationships  Helene Kergoat, None; Carl Dutrisac, None; John V. Lovasik, None
  • Footnotes
    Support  Natural Sciences and Engineering Research Council of Canada; Canadian Foundation for Innovation
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6835. doi:
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      Helene Kergoat, Carl Dutrisac, John V. Lovasik; Evaluation Of Retinal Vasomotor Reactivity During Changes In Arterial Blood Oxygen Content. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6835.

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

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Purpose: : To compare vasomotor responses to flicker across retinal quadrants during experimental changes in the arterial blood oxygen (O2) saturation level.

Methods: : The diameter of paired retinal arteries and veins was quantified with a Retinal Vessel Analyser in 15 healthy volunteers (20 to 30 years of age) before, during, and after short-term hyperoxia and hypoxia. Hyperoxic vasoconstriction was induced by inhaling 100% O2 while hypoxic vasodilation was elicited by inhaling 88% O2 in a balance of nitrogen. Vasomotor responses to 30sec of flicker were elicited during inhalation of normal room air and towards the end of inhaling either test gas. The O2 saturation level (SaO2), end-tidal carbon dioxide (EtCO2), pulse rate (PR) and respiratory rate (RR) were recorded throughout testing. The blood pressure and intraocular pressure were measured to calculate the ocular perfusion pressure (OPP). Statistics consisted of ANOVAs for alpha = 0.05.

Results: : Hyperoxia increased arterial SaO2 by 1.3% (p= 0.0001), decreased EtCO2 by 12.0% (p= 0.0001), reduced PR by 3.6% (p= 0.0001), increased OPP by 6.0% (p= 0.0001), had no effect on RR, but decreased the caliber of retinal arteries and veins by 9.3% and 14.3% respectively (p= 0.0001). In contrast, hypoxia decreased arterial SaO2 by 8.2% (p= 0.0001), decreased EtCO2 by 3.8% (p= 0.0042), increased PR by 14.6% (p= 0.0001), decreased OPP by 10.8% (p= 0.0001) and increased arterial and venous diameter by 5.7% and 5.1% (p= 0.0001) respectively. The changes in the vessel caliber were the same across quadrants. The amplitude of arterial/venous dilation to flicker at baseline increased by 1.5% and 1.8% respectively in hyperoxia (p< 0.02) and decreased by 2.0% and 1.7% respectively in hypoxia (p= 0.0001). The vasomotor changes were not uniform across all quadrants.

Conclusions: : While hyperoxia was associated with an increase in the vasomotor response, hypoxia was associated with a reduction in the amplitude of flicker-induced vasodilation. The reduced dilation was attributed to a structural limit for dilation beyond that caused by systemic hypoxia, or that the need for additional nutrients due to flicker was already satisfied.

Keywords: blood supply • hypoxia • retina 

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