Interactions of Fatty Acids with the Calcium Release Channel in Malignant Hyperthermia

  • Jeffrey E. Fletcher
  • Henry Rosenberg
  • Jill Beech
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 301)


The anesthesia-induced malignant hyperthermia (MH) syndrome has been suggested to be a consequence of a halothane-sensitive defect in Ca2+ regulation, based on muscle rigidity during the syndrome and the increase in Ca2+ in isolated fiber bundles exposed to halothane. Additionally, the threshold of Ca2+-induced Ca2+ release (TCICR) is lower than normal in isolated fractions of heavy sarcoplasmic reticulum (HSR) from porcine MH muscle.1,2 However, the defect need not reside in the Ca2+-release channel protein, as there are reports of nonrigid MH in humans3 and loss of Ca2+ regulation could be the result of a disturbance in fatty acid metabolism.4 The present study examines fatty acid metabolism and the influence of fatty acids on various aspects of Ca2+ regulation and on caffeine, halothane and succinylcholine action in normal and MH muscle. Additionally, since phenytoin has been suggested to antagonize MH,5 its effects on Ca2+ regulation and fatty acid metabolism have been examined.


Fatty Acid Metabolism Malignant Hyperthermia Malignant Hyperthermia Muscle Strip Porcine Muscle 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • Jeffrey E. Fletcher
    • 1
    • 2
  • Henry Rosenberg
    • 2
  • Jill Beech
    • 3
  1. 1.Departments of AnesthesiologyHahnemann UniversityPhiladelphiaUSA
  2. 2.Departments of BiochemistryHahnemann UniversityPhiladelphiaUSA
  3. 3.Department of Clinical StudiesUniversity of Pennsylvania School of Veterinary Medicine, New Bolton CenterKennett SquareUSA

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