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Muscle Mitochondria and Malignant Hyperthermia

  • Khay S. Cheah
Conference paper

Abstract

Malignant hyperthermia (MH) is a genetically inherited potentially fatal disorder affecting primarily the skeletal muscle of humans, stress-susceptible pigs, and, to a lesser extent, dogs. In MH-susceptible humans and animals, it is generally accepted that an increase in the level of myoplasmic free Ca2+ is the initiator of the syndrome [1–5]. Various hypotheses have been suggested to account for the increase in myoplasmic Ca2+, such as an excess formation of fatty acids [2,6,7], an abnormality in the excitation-contraction coupling mechanism [8], a defect in the Ca2+ release channel of the sarcoplasmic reticulum [9–11], free radical-mediated peroxidation of membrane lipids [12], and a lower than normal Mg2+ inhibition of the Ca2+ release channel of the sarcoplasmic reticulum [13]. However, considerable evidence also supports MH to be due to a widespread membrane defect affecting various organelles, for example, platelets, erythrocytes, lymphocytes, and mitochondria [review, 1,2,14,15], in addition to skeletal muscle.

Keywords

Sarcoplasmic Reticulum Malignant Hyperthermia Malignant Hyperthermia Muscle Mitochondrion Biopsy Skeletal 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

© Springer-Verlag Tokyo 1996

Authors and Affiliations

  • Khay S. Cheah
    • 1
  1. 1.Department of AgricultureThe University of MelbourneParkvilleAustralia

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