Abstract: The mechanism of respiratory inhibition of streptomycin was studied in the rats, rab- bits, and dogs. In the anaesthetized rabbits, intravenous injection of ammonium chloride neither prevented nor antagonized the respiratory insufficiency following intravenous ad- ministration of streptomycin. In some experiment, the caroid sinus area of one rabbit (recipient) was vascularly isolated and perfused by the arterial blood of another animal (donor). It was demonstrated that streptomycin given intravenously to the donor failed to provoke respiratory change of the recipient, while sodium cyanide given via the same route stimulated respiration in both rabbits. Furthermore streptomycin failed to influence the sodium cyanide hyperpnoea. Intracisteral injection of streptomycin in a dose of 720-14400 I.U./animal (total volume 0.18-0.20 ml) caused no changes of respiration. The mechanism of streptomycin was studied in cross-circulation experiment of dogs; the head circulation of the recipient dog was completely isolated from that of the body, and was perfused by the donor dog. When streptomycin, 70000 I.U./kg, was given to the head circulation via the donor animal, the recipient respiration did not change signifi- cantly, but respiratory paralysis of the recipient dog was induced by femoralis vena given to the recipient in the same dose of streptomycin. In the rabbits and rats, both the effects of respiratory inhibition and neuromuscular blockade of streptomycin were anta- gonized parallelly by intravenous injection of calcium chloride. It is suggested that the mechanism of respiratory inhibitory effect of streptomycin is related neither to the inhibitory effect on the central nervous system nor to that on the chemoreceptors of the carotid body, and that is chiefly due to the neuromuscular blokade: effect of streptomycin.