Effects of methacholine infusion on desflurane pharmacokinetics in piglets.

Alf Kozian,Anders Larsson,Moritz Kretzschmar,Jens Schreiber,Thomas Hachenberg,James E Baumgardner,Göran Hedenstierna,Thomas Schilling

doi:10.1016/j.dib.2015.11.002

Abstract

The data of a corresponding animal experiment demonstrates that nebulized methacholine (MCh) induced severe bronchoconstriction and significant inhomogeneous ventilation and pulmonary perfusion (V̇A/Q̇) distribution in pigs, which is similar to findings in human asthma. The inhalation of MCh induced bronchoconstriction and delayed both uptake and elimination of desflurane (Kretzschmar et al., 2015) [1].The objective of the present data is to determine V̇A/Q̇ matching by Multiple Inert Gas Elimination Technique (MIGET) in piglets before and during methacholine- (MCh-) induced bronchoconstriction, induced by MCh infusion, and to assess the blood concentration profiles for desflurane (DES) by Micropore Membrane Inlet Mass Spectrometry (MMIMS).Healthy piglets (n=4) under general anesthesia were instrumented with arterial, central venous, and pulmonary artery lines. The airway was secured via median tracheostomy with an endotracheal tube, and animals were mechanically ventilated with intermittent positive pressure ventilation (IPPV) with a FiO2 of 0.4, tidal volume (VT)=10 ml/kg and PEEP of 5cmH2O using an open system. The determination of V.A/Q. was done by MIGET: before desflurane application and at plateau in both healthy state and during MCh infusion. Arterial blood was sampled at 0, 1, 2, 5, 10, 20, and 30 min during wash-in and washout, respectively.Bronchoconstriction was established by MCH infusion aiming at doubling the peak airway pressure, after which wash-in and washout of the anesthetic gas was repeated. Anesthesia gas concentrations were measured by MMIMS. Data were analyzed by ANOVA, paired t-test, and by nonparametric Friedman׳s test and Wilcoxon׳s matched pairs test.We measured airway pressures, pulmonary resistance, and mean paO2 as well as hemodynamic variables in all pigs before desflurane application and at plateau in both healthy state and during methacholine administration by infusion. By MIGET, fractional alveolar ventilation and pulmonary perfusion in relation to the V.A/Q. compartments, data of logSDQ̇ and logSDV̇ (the second moments describing global dispersion, i.e. heterogeneity of distribution) were estimated prior to and after MCh infusion. The uptake and elimination of desflurane was determined by MMIMS.

Highlights

The data of a corresponding animal experiment demonstrates that nebulized methacholine (MCh) induced severe bronchoconstriction and significant inhomogeneous ventilation and pulmonary perfusion (V A/Q ) distribution in pigs, which is similar to findings in human asthma
The airway was secured via median tracheostomy with an endotracheal tube, and animals were mechanically ventilated with intermittent positive pressure ventilation (IPPV) with a FiO2 of 0.4, tidal volume (VT)1⁄4 10 ml/kg and
The determination of V A/Q was done by Multiple Inert Gas Elimination Technique (MIGET): before desflurane application and at plateau in both healthy state and during MCh infusion

Summary

Data accessibility

Text file, graph, figure Mass Spectrometry, Multiple Inert Gas Elimination Technique. Calculated and statistically analyzed data in tables and figures Respiratory physiology determined before desflurane application and at plateau in both healthy state and during methacholine infusion Multiple Inert Gas Elimination Technique allows the determination of ventilation and pulmonary perfusion distribution. Multiple Inert Gas Elimination Technique (MIGET) was used to determine alveolar ventilation and pulmonary perfusion distribution (V.A/Q.) before and during MCh infusion. MV minute ventilation, VT tidal volume; Paw airway pressure, Rtot total respiratory resistance, pa arterial partial pressure, SaO2 oxygen saturation in arterial blood, pv venous partial pressure, HR heart rate, MAP mean arterial pressure, MPAP mean pulmonary arterial pressure, CVP central venous pressure, CO cardiac output, PVR pulmonary vascular resistance, and SVR systemic vascular resistance (Fig. 1). A alveolar, V ventilation, Q perfusion, VD/VT dead space, and RSS remaining sum of squares

General

Animals

Anesthesia gas measurement by mass spectrometry

Findings

Data analysis