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1 Microhemodynamics, La Jolla Bioengineering Institute, La Jolla, CA, USA
2 Microhemodynamics, La Jolla Bioengineering Institute, La Jolla, CA, USA; Department of Bioengineering, University of California, San Diego, La Jolla, CA, USA
* To whom correspondence should be addressed. E-mail: pcabrales{at}ucsd.edu.
The rate of oxygen release from arterioles (~55 µm, diameter) was measured in the hamster window chamber model during flow and no flow conditions. Flow was stopped by microvascular transcutaneous occlusion using a glass pipette held by a manipulator. The reduction of the intra arteriolar oxygen tension (pO2) was measured by the phosphorescence quenching of pre-infused Pd-porphyrin, 100 µm down stream from the occlusion. Oxygen release from arterioles was found to be 53% greater during flow than no flow conditions (2.6 vs. 1.7 x 10-5 mlO2/cm2 sec, P < 0.05). Acute hemodilution with dextran 70 was used to reduce vessel oxygen content, significantly increase wall shear stress (14%, P < 0.05), reduce hematocrit (Hct) to 28.4 ± 1.0% (vs. 48.8 ± 1.8% at baseline), lowere oxygen supply by the arterioles (10%, P < 0.05) and increase oxygen release from the arterioles (39%, P < 0.05). Hemodilution also increased microcirculation oxygen extraction (33% greater than non hemodilution, P < 0.05) and oxygen consumption by the vessel wall, as shown by an increase in vessel wall oxygen gradient (difference in pO2 between the blood and the tissue side of the arteriolar wall, non hemodiluted 16.2 ± 1.0 vs. hemodiluted 18.3 ± 1.4 mmHg, P < 0.05). Oxygen released by the arterioles during flow vs. non flow was increased significantly after hemodilution (3.6 vs. 1.8 x 10-5 mlO2/cm2 sec, P < 0.05). The oxygen cost induced by wall shear stress, suggested by our findings, may be greater than 15% of the total oxygen delivery to tissues by arterioles during flow in this preparation.
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