REVERSIBILITY OF KANAMYCIN-INDUCED NEUROMUSCULAR AND CARDIOVASCULAR DEPRESSIONS BY 4-AMINOPYRIDINE, IN COMPARISON WITH NEOSTIGMINE

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It is known that aminoglycoside antibiotics can produce theneuromuscular blockade which is mainly based on their antireleasing action of acetylcholine (Ach) at neuromuscular junctions1, 2). The neuromuscular blocking actions of kanamycin sulfate (KM) were firstly reported in vivo by TIMMERMAN et al.3) and its presynaptic blocking action was suggested by SINGHet al.4). Furthermore, pre-and post-junctional blocking actions of KM were clearly showed in vitro, and it was confirmed that KM can act preferentially at the presynaptic site and that the antireleasing action of KM can be completely antagonized by 3, 4-diaminopyridine in vitro2)3, 4-Diaminopyridine can reverse the neuromuscular depression by amikacin5), polymyxin B, lincomycin and clindamycin6) in vitro and 4-aminopyridine (4-AP) can reverselincomycin-pancuronium-induced neuromuscular blockade in man7). KM has not only the neuromuscular blocking action but also the cardiovascular depressive action8)as have the other aminoglycoside antibiotics9, 10, 11, 12, 13).
The aim of this study was to examine whether, as in vitro experiments of neuromuscular system, 4-AP could antagonize the neuromuscular and cardiovascular depressive actions of KM in anesthetized rats.