Pancuronium Clindamycin

Clindamycin and hncomycin potentiate the action of nondepolarizing neuromuscular blocking drugs, such as pancuronium and D-tubocurarine. The lincosamide-induced block cannot be reliably reversed pharmacologically (71). 

Clinically important, potentially hazardous interactions with acetazolamide, aminoglycosides, anticholinesterases, bambuterol, calcium channel blockers, chloroquine, chlorpromazine, clindamycin, d-pencillamine, ecothiophate iodine, enflurane, furosemide, halothane, hexomethonium, isoflurane, ketamine, lidocaine, lincomycin, lithium salts, magnesium salts, mannitol, MAO inhibitors, organophosphates, pancuronium, phenytoin, polymyxins, procainamide, quinidine, sevoflurane, spectinomycin, tetracyclines... 

Electrolyte imbalance, and diseases that lead to electrolyte imbalance, such as adrenal cortical insufficiency, alter neuromuscular blockade. Depending on the nature of the imbalance, either enhancement or inhibition may be expected. Magnesium sulfate, used in the management of toxemia of pregnancy, enhances the skeletal-muscle-relaxing effects of pancuronium. Antibiotics such as aminoglycosides, tetracyclines, clindamycin, lincomycin, colistin, and sodium colistimethate augment the pancuronium-induced neuromuscular blockade. Anesthetics such as halothane, enflurane, and isoflurane enhance the action of pancuronium, whereas azathioprine will cause a reversal of neuromuscular blockade. 

FogdaU RP, MiUer RD. Prolongation of a pancuronium-induced neuromuscular blockade clindamycin. Anesthesiology (1974) 41, 407-8. 

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