P. Nouhnejad, A.R. Dehpour, T. Samadian, Sh. Amini
Aminoglycoside antibiotics are all capable of producing clinically significant neuromuscular paralysis.
Since part of the mechanism of action of these antibiotics at neuromuscular junction is a calciumdependent inhibition of acetylcholine release, so this experiment was carried out in vitro on both somatic (isolated rat phrenic-nerve hemidiaphragm) and autonomic neuro-effector transmission (guinea-pig ileum) using gentamicin and amikacin, to determine the calcium contents at this level.
Electron microscopic observations on gentamycinandlor amikacin-treated materials, using potassium pyroantimonate method suggest a reduction of internal calcium in nerve terminals of both preparations.
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