Abstract
While defects in the ryanodine receptor may in some cases be necessary to impart the potential for malignant hyperthermia (MH) susceptibility, these defects are not sufficient to account for the MH syndrome. Obvious examples include swine homozygous for the proposed ryanodine receptor arginine to cysteine #615 MH mutation that do not exhibit an MH reaction at a young age [1] and those that do not consistently exhibit a reaction even as an adult, despite the administration of more than adequate amounts of triggering agents [2].
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© 1996 Springer-Verlag Tokyo
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Fletcher, J.E., Wieland, S.J. (1996). Fatty Acids: Potentially Crucial Modulators of the Malignant Hyperthermia Syndrome. In: Morio, M., Kikuchi, H., Yuge, O. (eds) Malignant Hyperthermia. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68346-9_17
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DOI: https://doi.org/10.1007/978-4-431-68346-9_17
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