Isoflurane and sevoflurane precondition against neutrophil-induced contractile dysfunction in isolated rat hearts

The authors tested the hypothesis that pretreatment with isoflurane or sevoflurane can protect the heart against neutrophil-induced contractile dysfunction. Studies were conducted in buffer-perfused and paced isolated rat hearts. Left ventricular developed pressure served as an index of contractilit...

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Bibliographic Details
Published in:Anesthesiology (Philadelphia) 2004-03, Vol.100 (3), p.489-497
Main Authors: GUOCHANG HU, SALEM, M. Ramez, CRYSTAL, George J
Format: Article
Language:English
Subjects:
Anesthesia
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Anesthetics, Inhalation - pharmacology
Animals
Biological and medical sciences
Female
Glyburide - pharmacology
Heart - drug effects
In Vitro Techniques
Ischemic Preconditioning, Myocardial - methods
Isoflurane - pharmacology
Male
Medical sciences
Membrane Proteins - drug effects
Methyl Ethers - pharmacology
Myocardial Contraction - drug effects
Myocardial Contraction - physiology
Myocardium - pathology
Neutrophils - physiology
Peroxidase - metabolism
Pinacidil - pharmacology
Potassium Channel Blockers - pharmacology
Potassium Channels
Rats
Rats, Sprague-Dawley
Sevoflurane
Superoxides - metabolism
Vasodilator Agents - pharmacology
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Summary:The authors tested the hypothesis that pretreatment with isoflurane or sevoflurane can protect the heart against neutrophil-induced contractile dysfunction. Studies were conducted in buffer-perfused and paced isolated rat hearts. Left ventricular developed pressure served as an index of contractility. Pretreatment consisted of administration of 1.0 minimum alveolar concentration isoflurane or sevoflurane for 15 min followed by a 10-min washout and was performed in the absence and presence of the adenosine triphosphate-sensitive potassium channel inhibitor glibenclamide (10 microM). Polymorphonuclear neutrophils and platelet-activating factor were then added to the perfusate for 10 min, followed by 30 min of recovery. Neutrophil retention was assessed from the difference between those administered and collected in coronary effluent and measurements of myeloperoxidase in myocardial samples. Isolated hearts were also used to assess the effect of volatile anesthetic pretreatment on cardiac dysfunction caused by enzymatically generated superoxide. In additional studies, the authors evaluated the effect of volatile anesthetic pretreatment on the adherence of neutrophils to isolated rat aortic segments. Platelet-activating factor-stimulated neutrophils caused marked and persistent reductions (> 50%) in left ventricular developed pressure. Pretreatment with either isoflurane or sevoflurane abolished these effects, as well as the associated increases in neutrophil retention. Glibenclamide did not alter these actions of the anesthetics. Pretreatment with either volatile anesthetic attenuated the reductions in left ventricular developed pressure caused by exogenous superoxide and abolished the increases in neutrophil adherence in the aortic segments. Isoflurane and sevoflurane preconditioned the heart against neutrophil-induced contractile dysfunction. This action was associated with an inhibition to neutrophil adherence and likely involved an increased resistance of the myocardium to oxidant-induced injury; the adenosine triphosphate-sensitive potassium channels played no apparent role.
ISSN:0003-3022
1528-1175
DOI:10.1097/00000542-200403000-00006