HALOTHANE, ISOFLURANE, AND SEVOFLURANE REDUCE POSTISCHEMIC ADHESION OF NEUTROPHILS IN THE CORONARY SYSTEM

Citation
C. Kowalski et al., HALOTHANE, ISOFLURANE, AND SEVOFLURANE REDUCE POSTISCHEMIC ADHESION OF NEUTROPHILS IN THE CORONARY SYSTEM, Anesthesiology, 86(1), 1997, pp. 188-195
Citations number
33
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
86
Issue
1
Year of publication
1997
Pages
188 - 195
Database
ISI
SICI code
0003-3022(1997)86:1<188:HIASRP>2.0.ZU;2-K
Abstract
Background Polymorphonuclear neutrophils (PMNs) contribute to postisch emic reperfusion damage in many organs and tissues, a prerequisite bei ng adhesion of PMNs to vascular endothelial cells, Because adhesion pr ocesses involve orderly interactions of membrane proteins, it appeared possible that ''membrane effects'' of volatile anesthetics could inte rfere, We investigated the effects of halothane, isoflurane, and sevof lurane on postischemic adhesion of human PMNs in the intact coronary s ystem of isolated perfused guinea pig hearts, Methods: The hearts (n = 7-10 per group) were perfused in the ''Langendorff'' mode under condi tions of constant flow (5 ml/min) using modified Krebs-Henseleit buffe r equilibrated with 94.4% oxygen and 5.6% carbon dioxide, Global myoca rdial ischemia was induced by interrupting perfusion for 15 min, In th e second minute of reperfusion (5 ml/min), a bolus dose of 6 x 10(5) P MNs was injected into the coronary system, The number of cells reemerg ing in the coronary effluent was expressed as a percentage of the tota l number of applied PMNs. Halothane, isoflurane, and sevoflurane, each at 1 and 2 minimal alveolar concentration (MAC), were vaporized in th e gas mixture and applied from 14 min before ischemia until the end of the experiment, Results: Under nonischemic conditions, 24.7 +/- 1.3% of the injected neutrophils did not reemerge from the perfused coronar y system, Subjecting the hearts to global ischemia augmented retention (36.4 +/- 2.8%, P <.05), Application of halothane reduced adhesion of neutrophils to 22.6 +/- 2.1% and 24.2 +/- 1.8% at 1 and 2 MAC, respec tively (P <.05). Exposure to 1 and 2 MAC isoflurane was similarly effe ctive, whereas basal adhesion was not significantly influenced, Sevofl urane-treated hearts (1 and 2 MAC) also showed decreased adhesion of P MNs (23 +/- 2.3% and 24.8 +/- 1.8%, respectively; P < .05) and an iden tical reduction resulted when sevoflurane (1 MAC) was applied only wit h the onset of reperfusion. Conclusions: Although the mechanism of act ion of volatile anesthetics remains unclear in these preliminary studi es, their inhibitory effect on ischemia-induced adhesion of PMNs may b e beneficial for the heart during general anesthesia.