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, blood/muscle lactate levels, plasma potassium, acid-base balance. Three treatment protocols had two phases each: A-1, discontinue halothane, inject dantrolene 7.5 mg X kg-1; A-2, inject HCO3- (113 +/- 6 mEq). B-1, Discontinue halothane, inject HCO3- (118 +/- 13 mEq); B-2, inject dantrolene 7.5 mg X kg-1; X C-1, Continue halothane, inject dantrolene 7.5 mg X kg-1; C-2, discontinue halothane, inject HCO3- (101 +/- 8 mEq). Dantrolene and HCO3- acted separately and differently: dantrolene reversed the hypermetabolism, both aerobic and anerobic, and HCO3- reversed the extracellular metabolic acidosis. Semitendinosus muscle biopsies demonstrated that both red and white muscle are involved in MH, that muscle lactate (to 35 mumol X g-1) consistently exceeded blood lactate (to 22 mumol X ml-1), and that 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.