Halothane-induced porcine malignant hyperthermia: metabolic and hemodynamic changes.
Metabolic, hemodynamic and neuroendocrine responses to halothane were measured in five normal and five malignant hyperthermia-susceptible (MHS) swine. Constant-volume ventilation was used. There was no therapeutic intervention. In NHS animals, blood lactate concentrations increased first, and the initial increases appeared to be non-hypoxic in origin. Lactate concentrations increased progressively to more than 20 mum/ml. Whole-body oxygen consumption increased almost twofold, and hind limb muscle oxygen consumption increased almost threefold. Extrapolated increases in muscle oxygen consumption accounted for about 55 per cent of the increase in whole-body oxygen consumption. Respiratory and metabolic acidosis, marked hyperkalemia, and increases in catecholamines and temperature occurred secondarily and were accompanied by progressive circulatory failure.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000187:drug effects; D004837:Epinephrine / Q000097:blood; D006221:Halothane / Q000009:adverse effects*; D006439:Hemodynamics / Q000187:drug effects*; D007773:Lactates / Q000097:blood; D008305:Malignant Hyperthermia / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D013552:Swine
D007773:Lactates; D002245:Carbon Dioxide; D010100:Oxygen; D006221:Halothane; D009638:Norepinephrine; D004837:Epinephrine