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1 Division of General and Surgical Intensive Care Medicine, Department of Anesthesia and Critical Care Medicine, The Leopold-Franzens-University of Innsbruck, Innsbruck, Austria
2 Krankenhaus der Barmherzigen Schwestern, Ried I. Innkreis, Austria
3 Department of Bioengineering, University of California, San Diego, La Jolla, CA, USA
* To whom correspondence should be addressed. E-mail: barbara.friesenecker{at}uibk.ac.at.
The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during Argininevasopressin (AVP) induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU/kg/min) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural pO2 difference. AVP caused tissue pO2 to be significantly lowered from 25.4 ± 7.4 mmHg to 7.2 ± 5.8 mmHg, however total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue pO2 and increased wall oxygen concentration gradient are compatible with the hypothesis that vasoconstriction significantly increases vessel wall oxygen consumption, which in this model appears to constitute an important oxygen consuming compartment. This conclusion was supported by the finding that a small percentage of the vessels that in these experiments dilated had a vessel wall oxygen gradient that was smaller than control, and which was not determined by changes in tissue pO2. These finding show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation.
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