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CARDIOVASCULAR ANESTHESIA

The Impact of Isoflurane During Simulated Ischemia/Reoxygenation on Intracellular Calcium, Contractile Function, and Arrhythmia in Ventricular Myocytes

Martin Dworschak, MD^*,, Dirk Breukelmann, MD^*,, and James D. Hannon, MD^*

*Department of Anesthesia Research, Mayo Clinic, Rochester, Minnesota, Division of Cardiothoracic and Vascular Anaesthesia and Intensive Care, University Hospital Vienna, Austria, and Department of Anaesthesiology and Intensive Care, University of Münster, Germany

Address correspondence and reprint requests to Martin Dworschak, MD, Division of Cardiothoracic Anesthesia and Intensive Care, University Hospital Vienna, Waehringer Guertel 18–20, A-1090 Vienna, Austria. Address email to martin.dworschak{at}univie.ac.at

Some of isoflurane’s cellular actions, such as interference with intracellular Ca²⁺ handling, inhibition of the respiratory chain, and the capability to produce oxygen radicals, could result in impaired cellular function during ischemia/reoxygenation (I/R). We investigated the effects of isoflurane applied during I/R on intracellular Ca²⁺, oxygen radical formation, arrhythmic events, and contractile function in rat cardiomyocytes. Single ventricular myocytes were subjected to 30 min of simulated ischemia followed by 30 min of reoxygenation. After baseline measurements, isoflurane-treated cells were exposed to 1 minimum alveolar concentration of isoflurane in air, whereas control cells were exposed to air only. Cytosolic Ca²⁺ overload was observed in the isoflurane group (P < 0.05). During ischemia, systolic cell shortening decreased in both groups. In the isoflurane group, arrhythmic events and hypercontracture occurred more often during I/R, and the recovery of contractility during reoxygenation was less marked (P < 0.05). Furthermore, increased oxygen radical generation was detected in isoflurane-treated myocytes during reoxygenation (P < 0.05). Isoflurane given during I/R in this study induced intracellular Ca²⁺ accumulation and impaired cell function. These potentially harmful effects were associated with a diminished Ca²⁺ clearance and an accelerated oxygen radical production.

IMPLICATIONS: Isoflurane, a volatile anesthetic, administered during ischemia/reoxygenation, aggravated functional impairment in heart muscle cells. These alterations were probably caused by interference with intracellular Ca²⁺ handling proteins and by generation of oxygen radicals. Cardioprotection by isoflurane when given before ischemia should be reevaluated in situations of continuing ischemia and subsequent reperfusion.

This article has been cited by other articles:

				M. Dworschak, L. V. d'Uscio, D. Breukelmann, and J. D. Hannon Increased tolerance to hypoxic metabolic inhibition and reoxygenation of cardiomyocytes from apolipoprotein E-deficient mice Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H160 - H167. [Abstract] [Full Text] [PDF]

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