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Dantrolene (see Chapter 29 ), a drug used for the treatment of malignant hyperthermia, prevents Ca2+ release from the sarcoplasmic reticulum and blocks excitation-contraction coupling. Although it does not block neuromuscular transmission, the mechanical response to stimulation will be depressed without demonstrating any effect on the electromyogram.[547] [548] The effects of nondepolarizing neuromuscular blockers are enhanced by dantrolene. [157]
Azathioprine, an immunodepressant drug used in renal transplantation, has a minor antagonistic action on muscle relaxant-induced neuromuscular blockade. [549] [550]
Steroids antagonize the effects of nondepolarizing neuromuscular blockers in humans.[551] [552] Animal studies have also demonstrated resistance to the effects of dTc in the presence of prednisolone, dexamethasone, betamethasone, and triamcinolone.[553] [554] [555] Possible mechanisms for this interaction include (1) facilitation of acetylcholine release as a result of the effect of steroids on the presynaptic motor nerve terminal[556] or (2) channel blockade of the nAChR.[557] It should be noted that endogenous steroids act noncompetitively on nAChRs.[558] Prolonged treatment—combining corticosteroids with neuromuscular blocking drugs—can result in prolonged weakness (see the section "Neuromuscular Blockers and Weakness Syndromes in the Critically Ill").
Antiestrogenic drugs such as tamoxifen appear to potentiate the effects of nondepolarizing neuromuscular blockers.[559]
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