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

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

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

Content Provider	Springer Nature : BioMed Central
Author	Schuster, Frank Müller, Rainer Hartung, Edmund Roewer, Norbert Anetseder, Martin
Abstract	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. 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 μM, 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. 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. 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.
Related Links	https://bmcanesthesiol.biomedcentral.com/counter/pdf/10.1186/1471-2253-5-8.pdf
Ending Page	5
Page Count	5
Starting Page	1
File Format	HTM / HTML
ISSN	14712253
DOI	10.1186/1471-2253-5-8
Journal	BMC Anesthesiology
Issue Number	1
Volume Number	5
Language	English
Publisher	BioMed Central
Publisher Date	2005-06-09
Access Restriction	Open
Subject Keyword	Anesthesiology Internal Medicine Emergency Medicine Intensive Critical Care Medicine Halothane Sarcoplasmic Reticulum Ryanodine Receptor Malignant Hyperthermia
Content Type	Text
Resource Type	Article
Subject	Anesthesiology and Pain Medicine
Journal Impact Factor	2.3/2023
5-Year Journal Impact Factor	2.6/2023

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