Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction

1 Division of General and Surgical Intensive Care Medicine, Department of Anesthesia and Critical Care Medicine, The Leopold-Franzens-University of Innsbruck, A-6020 Innsbruck, Austria; 2 Department of Bioengineering, University of California, San Diego; La Jolla, California 92093-0412; and 3 Krankenhaus der Barmherzigen Schwestern, A-4910 Ried I Innkreis, Austria Submitted 2 June 2004 ; accepted in final form 10 June 2004 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 arginine vasopressin (AVP)-induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU·kg –1 ·min –1 ) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural P O 2 difference. AVP caused tissue P O 2 to be significantly lowered from 25.4 ± 7.4 to 7.2 ± 5.8 mmHg; however, total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue P O 2 , 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 the small percentage of the vessels that dilated in these experiments had a vessel wall oxygen gradient that was smaller than control and which was not determined by changes in tissue P O 2 . These findings show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation. vasoactivity; oxygen gradients; tissue oxygenation; vasomotion; metabolism Address for reprint requests and other correspondence: B. Friesenecker, Div. of General and Surgical Intensive Care Medicine, Dept. of Anesthesia and Critical Care Medicine, The Leopold-Franzens Univ. of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria (E-mail: barbara.friesenecker{at}uibk.ac.at )