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Schuster F, Müller R, Hartung E, et al. Inhibition of sarcoplasmic Ca2+-ATPase increases caffeine- and halothane-induced contractures in muscle bundles of malignant hyperthermia susceptible and healthy individuals. BMC Anesthesiol. 2005;5:8doi: 10.1186/1471-2253-5-8.
Schuster, F., Müller, R., Hartung, E., Roewer, N., & Anetseder, M. (2005). Inhibition of sarcoplasmic Ca2+-ATPase increases caffeine- and halothane-induced contractures in muscle bundles of malignant hyperthermia susceptible and healthy individuals. BMC anesthesiology, 58. https://doi.org/10.1186/1471-2253-5-8
Schuster, Frank, et al. "Inhibition of sarcoplasmic Ca2+-ATPase increases caffeine- and halothane-induced contractures in muscle bundles of malignant hyperthermia susceptible and healthy individuals." BMC anesthesiology vol. 5 (2005): 8. doi: https://doi.org/10.1186/1471-2253-5-8
Schuster F, Müller R, Hartung E, Roewer N, Anetseder M. Inhibition of sarcoplasmic Ca2+-ATPase increases caffeine- and halothane-induced contractures in muscle bundles of malignant hyperthermia susceptible and healthy individuals. BMC Anesthesiol. 2005 Jun 09;5:8. doi: 10.1186/1471-2253-5-8. PMID: 15946384; PMCID: PMC1175794.
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BMC Anesthesiol. 2005 Jun 09;5:8. doi: 10.1186/1471-2253-5-8.

Inhibition of sarcoplasmic Ca2+-ATPase increases caffeine- and halothane-induced contractures in muscle bundles of malignant hyperthermia susceptible and healthy individuals.

BMC anesthesiology

Frank Schuster, Rainer Müller, Edmund Hartung, Norbert Roewer, Martin Anetseder

Affiliations

  1. Department of Anaesthesiology, University of Wuerzburg Oberduerrbacher Strasse 6, 97080 Wuerzburg, Germany. [email protected]

PMID: 15946384 PMCID: PMC1175794 DOI: 10.1186/1471-2253-5-8

Abstract

BACKGROUND: Malignant hyperthermia (MH) is triggered by halogenated anaesthetics and depolarising muscle relaxants, leading to an uncontrolled hypermetabolic state of skeletal muscle. An uncontrolled sarcoplasmic Ca2+ release is mediated via the ryanodine receptor. A compensatory mechanism of increased sarcoplasmic Ca2+-ATPase activity was described in pigs and in transfected cell lines. We hypothesized that inhibition of Ca2+ reuptake via the sarcoplasmic Ca2+-ATPase (SERCA) enhances halothane- and caffeine-induced muscle contractures in MH susceptible more than in non-susceptible skeletal muscle.

METHODS: With informed consent, surplus muscle bundles of 7 MHS (susceptible), 7 MHE (equivocal) and 16 MHN (non-susceptible) classified patients were mounted to an isometric force transducer, electrically stimulated, preloaded and equilibrated. Following 15 min incubation with cyclopiazonic acid (CPA) 25 microM, the European MH standard in-vitro-contracture test protocol with caffeine (0.5; 1; 1.5; 2; 3; 4 mM) and halothane (0.11; 0.22; 0.44; 0.66 mM) was performed. Data as median and quartiles; Friedman- and Wilcoxon-test for differences with and without CPA; p < 0.05.

RESULTS: Initial length, weight, maximum twitch height, predrug resting tension and predrug twitch height of muscle bundles did not differ between groups. CPA increased halothane- and caffeine-induced contractures significantly. This increase was more pronounced in MHS and MHE than in MHN muscle bundles.

CONCLUSION: Inhibition of the SERCA activity by CPA enhances halothane- and caffeine-induced contractures especially in MHS and MHE skeletal muscle and may help for the diagnostic assignment of MH susceptibility. The status of SERCA activity may play a significant but so far unknown role in the genesis of malignant hyperthermia.

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