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Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Retinal arteriolar and middle cerebral artery responses to combined hypercarbic/hyperoxic stimuli.
Investigative Ophthalmology & Visual Science 2008 December
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 (P(ET)O(2)) 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 P(ET)O(2) 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 P(ET)O(2).
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 (P(ET)O(2)) 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 P(ET)O(2) 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 P(ET)O(2).
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