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Am J Physiol Heart Circ Physiol 288: H1515-H1520, 2005. First published November 24, 2004; doi:10.1152/ajpheart.00955.2004
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Microvascular oxygen delivery and consumption following treatment with verapamil

Nanae Hangai-Hoger,1 Amy G. Tsai,1,2 Barbara Friesenecker,3 Pedro Cabrales,1,2 and Marcos Intaglietta1,2

1Department of Bioengineering, University of California, San Diego, 2La Jolla Bioengineering Institute, La Jolla, California; and 3Division of General and Surgical Intensive Care Medicine, Department of Anesthesia and Critical Care Medicine, Leopold-Franzens-University of Innsbruck, Innsbruck, Austria

Submitted 13 September 2004 ; accepted in final form 22 November 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 relaxation to oxygen consumption of the microvascular wall during verapamil-induced vasodilatation. Verapamil HCl delivered in a 0.1 mg/kg bolus injection followed by a continuous infusion of 0.01 mg·kg–1·min–1 caused significant arteriolar dilatation, increased microvascular flow and functional capillary density, and decreased arteriolar vessel wall transmural PO2 difference. Verapamil caused tissue PO2 to increase from 25.5 ± 4.1 mmHg under control condition to 32.0 ± 3.7 mmHg during verapamil treatment. Total oxygen released by the microcirculation to the tissue remained the same as at baseline. Maintenance of the same level of oxygen release to the tissue, increased tissue PO2, and decreased wall oxygen concentration gradient are compatible if vasodilatation significantly lowers vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. These findings show that treatment with verapamil, which increases oxygen supply through vasodilatation, may further improve tissue oxygenation by lowering oxygen consumption of the microcirculation.

vasoactivity; oxygen gradients; tissue oxygenation; microvessel metabolism



Address for reprint requests and other correspondence: N. Hangai-Hoger, Dept. of Bioengineering, 0412, Univ. of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093-0412 (E-mail: nhangai{at}bioeng.ucsd.edu)




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