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Titolo:
ATX II, a sodium channel toxin, sensitizes skeletal muscle to halothane, caffeine, and ryanodine
Autore:
Fletcher, JE; Adnet, PJ; Reyford, H; Wieland, SJ; Stewart, SL; Rosenberg, H;
Indirizzi:
Trin Commun, Conshohocken, PA 19428 USA Trin Commun Conshohocken PA USA 19428 Commun, Conshohocken, PA 19428 USA
Titolo Testata:
ANESTHESIOLOGY
fascicolo: 5, volume: 90, anno: 1999,
pagine: 1294 - 1301
SICI:
0003-3022(199905)90:5<1294:AIASCT>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
MALIGNANT HYPERTHERMIA SUSCEPTIBILITY; HYPERKALEMIC PERIODIC PARALYSIS; AGONIST BAY K-8644; CONTRACTURE-TEST; SARCOPLASMIC-RETICULUM; GENETIC-HETEROGENEITY; DIAGNOSIS; RECEPTOR; CALCIUM; INVITRO;
Keywords:
gender; muscle rigidity; myotonia; succinylcholine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Fletcher, JE Trin Commun, 4 Tower Bridge,200 Barr Harbor Dr, Conshohocken,PA 19428 USA Trin Commun 4 Tower Bridge,200 Barr Harbor Dr Conshohocken PAUSA 19428
Citazione:
J.E. Fletcher et al., "ATX II, a sodium channel toxin, sensitizes skeletal muscle to halothane, caffeine, and ryanodine", ANESTHESIOL, 90(5), 1999, pp. 1294-1301

Abstract

Background: The function or expression of subtypes of the sodium ion (Na+)channel is altered In biopsies or cultures of skeletal muscle from many persons who are susceptible to malignant hyperthermia (MH), ATX II, a specific Na+ channel toxin from a sea anemone, causes delayed inactivation of the channel similar to that seen in cell cultures of MH muscle. ATX II was added to skeletal muscle to determine whether altered Na+ channel function could increase the sensitivity of normal skeletal muscle to agents (halothane, caffeine, ryanodine) to which MH muscle is hypersensitive. Methods: Studies were performed of fiber bundles from the vastus lateralismuscle of persons who were deemed not MH susceptible (MH-) or MH susceptible (MH+) according to the MH diagnostic test and of strips of diaphragm muscle from rats. Preparations in a tissue bath containing Krebs solution wereconnected to a force transducer, ATX II was introduced 5 min before halothane, caffeine, or ryanodine,Results: ATX II increased the magnitude of contracture to halothane in preparations from most MH-, but not MH+, human participants. After ATX LI treatment, preparations from 9 of 24 MH- participants generated contractures tohalothane, 3%, that were of the same magnitude as those from MH+ participants, Preparations from four of six ATX ii-treated healthy participants alsogave responses of the same magnitude as those of MH-susceptible participants to a graded halothane challenge (0.5-3%). The contractures to bolus doses of halo thane in specimens from male participants were more than three times larger than the contractures in specimens from female participants. In rat muscle, ATX II increased the magnitude of contracture to caffeine (2 mM) and decreased the time to produce a 1-g contracture to ryanodine (1 mu M). Conclusions: ATX II, which causes delayed inactivation of the Na+ channel in cell cultures similar to that reported in cultures of MH+ skeletal muscle, Increased the sensitivity of normal muscle to three agents to which MH+ muscle is hypersensitive. The increased sensitivity to halothane, 3%, occurred in most (79%), but not all, MH- participants, and this effect was most evident in male participants, There-fore, abnormal function of the Na+ channel, even if it is a secondary event in MH, may contribute to a positive contracture test result for MH.

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Documento generato il 26/01/20 alle ore 01:03:54