• Respir Physiol Neurobiol · Jan 2016

    Bronchoconstriction induced by inhaled methacholine delays desflurane uptake and elimination in a piglet model.

    • Moritz Kretzschmar, Alf Kozian, James E Baumgardner, Jens Schreiber, Göran Hedenstierna, Anders Larsson, Thomas Hachenberg, and Thomas Schilling.
    • Research Anesthesiologist, Department of Surgical Sciences, Hedenstierna Laboratory, Uppsala University, Uppsala, Sweden; Department of Anesthesiology and Intensive Care Medicine, Otto-von-Guericke-University Magdeburg, Germany.
    • Respir Physiol Neurobiol. 2016 Jan 1; 220: 88-94.

    AbstractBronchoconstriction is a hallmark of asthma and impairs gas exchange. We hypothesized that pharmacokinetics of volatile anesthetics would be affected by bronchoconstriction. Ventilation/perfusion (VA/Q) ratios and pharmacokinetics of desflurane in both healthy state and during inhalational administration of methacholine (MCh) to double peak airway pressure were studied in a piglet model. In piglets, MCh administration by inhalation (100 μg/ml, n=6) increased respiratory resistance, impaired VA/Q distribution, increased shunt, and decreased paO2 in all animals. The uptake and elimination of desflurane in arterial blood was delayed by nebulization of MCh, as determined by Micropore Membrane Inlet Mass Spectrometry (wash-in time to P50, healthy vs. inhalation: 0.5 min vs. 1.1 min, to P90: 4.0 min vs. 14.8 min). Volatile elimination was accordingly delayed. Inhaled methacholine induced severe bronchoconstriction and marked inhomogeneous VA/Q distribution in pigs, which is similar to findings in human asthma exacerbation. Furthermore, MCh-induced bronchoconstriction delayed both uptake and elimination of desflurane. These findings might be considered when administering inhalational anesthesia to asthmatic patients.Copyright © 2015 Elsevier B.V. All rights reserved.

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