Abstract
OBJECTIVE: We investigated the distribution of the partial pressure of oxygen in the tissue of un-anesthetize hamster window chamber model during anemic conditions (a hematocrit reduction of 40%) at breeding room air and normobaric hyperoxia. DESIGN AND METHODS: Acute hemodilution was induced by exchanging 40% of the animals estimated blood volume (7% of body weight) with dextran 70 kDa (B. Braun, Irvine, CA). Inspired oxygen (FiO(2)) concentration was either 21% or 100% at normobaric conditions. Systemic and microvascular hemodynamics were studied at each FiO(2), including blood pressure (BP), heart rate (HR), hematocrit (Hct), hemoglobin (Hb), blood gases, arteriolar and venular diameters and blood flow, and number of capillaries with red blood cells passage (functional capillary density, FCD). High resolution microvascular intravascular and interstitial pO(2) measurements were made using phosphorescence quenching microscopy (PQM). RESULTS: Hemodilution decreased Hct from 43% to 25%, with no systemic hemodynamic effects, although microcrovascular blood flow increased. Change in FiO(2) at baseline Hct increases arterial pO(2) with no significant effects on BP and HR, and decreased arteriolar diameter and blood flow. Measurement of interstitial pO(2) by scanning the tissue along set paths without regard to microvascular structures have a Gaussian distribution (mean ± SD, mmHg): 29.6 ± 5.7 (43% Hct, FiO(2) 0.21); 32.0 ± 10.5(43% Hct, FiO(2) 1.00); 31.12 ± 8.0 (25% Hct, FiO(2) 0.21); 26.0 ± 11.3 (25% Hct, FiO(2) 1.00). The decrease of oxygen carrying capacity by 40% reduced pO(2), paradoxically, the increased FiO(2) did not increase the average tissue pO(2) in the window chamber. All changes are statistically significant relative to baseline, p < 0.05.. CONCLUSIONS: At normal Hct values and during moderate hemodilution hyperoxia-induced vasoconstriction impairs microvascular oxygen transport and tissue oxygenation in the peripheral microcirculation.