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N₂O Modification of Halothane-Altered Renal Function in the Dog

GARY E. HILL, MD^*, JUDD K. LUNN, MD^*, MICHAEL R. HODGES, THEODORE H. STANLEY, MD, CRAIG R. SENTKER, BS^||, RICHARD JOHANSEN^**, and JOAN HATT^**

*Fellow in Anesthesiology, Department of Anesthesiology, The University of Utah College of Medicine, Salt Lake City, Utah 84132. Technical Research Supervisor, Department of Anesthesiology, The University of Utah College of Medicine, Salt Lake City, Utah 84132. Associate Professor of Anesthesiology/Surgery, Department of Anesthesiology, The University of Utah College of Medicine, Salt Lake City, Utah 84132. ||Research Systems Analyst, Department of Anesthesiology, The University of Utah College of Medicine, Salt Lake City, Utah 84132. **Research Assistant, Department of Anesthesiology, The University of Utah College of Medicine, Salt Lake City, Utah 84132.

Abstract

The influence on renal function of halothane (0.9%) in O₂ and of halothane, plus increasing concentrations (20, 40 and 60%) of N₂ or N₂O, was determined in 23 dogs. Halothane produced significant reductions in cardiac output and mean arterial pressure (MAP), which were not significantly further altered by addition of any concentration of N₂ or N₂0. Halothane in 0₂ caused marked reductions in urine flow rate and para-aminohippurate clearance (C_pah), inuline (C_in), and osmolar (C_osm) clearances, and significantly reduced free water clearance (Ch₂o) and renal blood flow (RBF). Urine osmolarity and renal vascular resistance (RVR) were significantly elevated by halothane-O₂. Addition of N₂0 produced further concentration-related reductions in urine flow rate, Ch₂o, and RBF. N₂O increased C_osm, urine osmolarity, and C_in but did not further alter C_pah or RVR. Addition of N₂ caused no further changes in urine flow rate, C_pah, C_in, C_osm, Ch₂o, RBF, urine osmolarity, or RVR. Maintenance of halothane (0.9%) in O₂ for 140 minutes in 5 dogs caused no further changes in renal function after the initially observed alterations. These data demonstrate that N-0 supplementation potentiates the antidiuresis produced by halothane and suggests that one mechanism involved may be stimulation of antidiuretic hormone release.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999