IOVS British Journal of Pharmacology
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Originally published In Press as doi:10.1167/iovs.08-1854 on May 23, 2008
(Investigative Ophthalmology and Visual Science. 2008;49:5503-5509.)
© 2008 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.08-1854

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Retinal Arteriolar and Middle Cerebral Artery Responses to Combined Hypercarbic/Hyperoxic Stimuli

Mila Kisilevsky,1 Alexandra Mardimae,2 Marat Slessarev,2 Jay Han,2 Joseph Fisher,2 and Chris Hudson1,3

1From the Departments of Ophthalmology and Vision Science and 2Anesthesiology, University of Toronto, Toronto, Ontario, Canada; and the 3School of Optometry, University of Waterloo, Waterloo, Ontario, Canada.

PURPOSE. The relative effect of simultaneously administered oxygen and carbon dioxide on the retinal and cerebral vessels is still controversial. The purpose of this study was to quantify and compare the superior-temporal retinal arteriole (RA) and middle cerebral artery (MCA) responses to hypercarbic and combined hypercarbic/hyperoxic stimuli.

METHODS. Twelve young, healthy volunteers participated in the study. End-tidal pressure of carbon dioxide was raised and maintained at 22% from baseline (hypercarbia), while end-tidal pressures of oxygen (PETO2) of 100 (normoxia), 500, and 300 mm Hg (hyperoxia) were instituted. RA diameter and blood velocity were measured with laser Doppler velocimetry and simultaneous vessel densitometry; MCA blood velocity was measured with transcranial Doppler ultrasound.

RESULTS. Normoxic hypercarbia increased RA blood velocity by +17% and calculated flow by +21%. Hypercarbia/hyperoxia-500 mm Hg decreased RA diameter by –8%, velocity by –16% and calculated flow by –29%. MCA blood velocity increased by +45% in response to normoxic hypercarbia, significantly greater than RA blood velocity (P < 0.001). Increase in PETO2 did not affect the hypercarbia-induced increase in MCA blood velocity.

CONCLUSIONS. Hyperoxia reversed hypercarbia-induced vasodilation in RA in a concentration-dependent manner. Hypercarbia induced greater vasodilation in the MCA than in the RA but MCA blood velocity was unaffected by increases in PETO2.








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