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Microvascular oxygen distribution in awake hamster window chamber model during hyperoxia

¹Department of Bioengineering, University of California, San Diego, La Jolla 92093-0412; and ²Sangart Inc., San Diego, California 92121

Submitted 23 February 2003 ; accepted in final form 22 May 2003

The microvascular effects and hemodynamic events following exposure to normobaric hyperoxia (because of inspiration of 100% O₂) were studied in the awake hamster window chamber model and compared with normoxia. Hyperoxia increased arterial blood PO₂ to 477.9 ± 19.9 from 60.0 ± 1.2 mmHg (P < 0.05). Heart rate and blood pressure were unaltered, whereas cardiac index was reduced from 196 ± 13 to 144 ± 31 ml · min^–1 · kg^–1 (P < 0.05) in hyperoxia. Direct measurements in the microcirculation showed there was arteriolar vasoconstriction, reduction of microvascular flow (83% of control, P < 0.05), and functional capillary density (FCD, 74 ± 16% of control), the latter change being significant (P < 0.05). Calculations of oxygen delivery and oxygen consumption based on the measured changes in microvascular blood flow velocity and diameter and estimates of oxygen saturation corrected for the Bohr effect due to the lowered pH and increased PCO₂ showed that oxygen transport in the microvascular network did not change between normal and hyperoxic condition. The congruence of systemic and microvascular hemodynamics events found with hyperoxia suggests that the microvascular findings are common to most tissues in the organism, and that hyperoxia, due to vasoconstriction and the decrease of FCD, causes a maldistribution of perfusion in the microcirculation.

functional capillary density; oxygen consumption; microvascular regulation

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