Abstract
Treatment of MH was studied in 21 pigs, using an isolated perfused caudal body preparation (L1 transection). Halothane one per cent triggered MH; data included oxygen consumption, bloodlmuscle lactate levels, plasma potassium, acid-base balance. Three treatment protocols had two phases each: A-1, discontinue halothane, injectdantrolene 7.5 mg.kg-1; A-2, inject HCO-2 (113 ± 6 mEq). B-l, Discontinue halothane, inject HCO-3 (118 ± 13 mEq);B-2, injectdantrolene 7.5 mg.kg-1. C-1, Continue halothane. inject dantrolene 7.5 mg-kg-1: C-2, discontinue halothane, inject HCO-3 (101 ± S mEq). Dantrolene and HCO-3 acted separately and differently: dantrolene reversed the hypermelabolism, both aerobic and anerobic, and HCO-3 reversed the extracellular metabolic acidosis. Semitendinosus muscle biopsies demonstrated that both red and white muscle are involved in MH, that muscle lactate (to 35 μmol.g-1 ) consistently exceeded blood lactate (to22 μmol-ml-1), andthat blood lactate levels were slow to diminish following treatment. One could expect continued release of muscle lactate into blood, despite adequate therapy of MH; this might suggest a recurrence even when such is not the case.
Résumé
Le traitement de l’hyperlhermie maligne a été étudié chez 21 cochons, utilisant une préparation de perfusion caudale isolée (transection LI). Un pour cent d’halothane a déclenché l’hyperthermie maligne; les données recueillies inclus la consommation d’oxygène, le niveau de lactate dans le sang/muscle, te potassium sérique et la balance acido-basique. Trois protocoles de traitement avaient chacun deux phases: A-1) V arrêt de V halothane, l’injection de dantrolène 7.5 mg.kg-1’;A-2) l’injection de HCO-3 (113 ± 6 mEq). B-I) l’arrêt de l’halothane, l’injection de l’HCO-3 (118 ± 13 mEq); B-2) l’injection de dantrolène 7.5 mg.kg-1. C-I) continue l’halothane, l’injection de dantrolène 7.5mg.kg-1; C-2) a cessé l’halothane, l’injection de HCO-3 (101 ± 8 mEq). Le dantrolène et le HCO-3 ont agi séparément et différemment: le dantrolène a renversé l’hypermêtabolisme, tant aérobique qu’anérobique, et le HCO-3 a renversé l’acidose métabolique extracellulaire. Les biopsies du muscle ont démontré que les deux groupes de muscles rouge et blanc sont impliqués dans l’hyperthermie maligne, que le lactate des muscles (35μmol.g-1) était constamment plus élevé que lactate sérique (22 μmol.ml-1), et que les niveaux sériques de lactate tardaient à diminuer après traitement. On pourrait s’attendre à une libération continue du lactate musculaire dans le sang, malgré une thérapie adéquate de l’hyperthermie maligne pouvant suggérer une rechute même si ce n’est pas le cas.
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Supported in part by GM 21729, National Institutes of Health, U.S. Public Health Service.
Dr. Ahern was supported in part by a Wellcome Trust Travel Grant.
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Gronert, G.A., Ahern, C.P. & Milde, J.H. Treatment of porcine malignant hyper-thermia: lactate gradient from muscle to blood. Can Anaesth Soc J 33, 729–736 (1986). https://doi.org/10.1007/BF03027122
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DOI: https://doi.org/10.1007/BF03027122