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在不均匀牵拉的离体大鼠膈肌标本上观察了氨基甙类抗菌素新霉素和链霉对终板电位(EPP)和微终板电位(MEPP)的影响和对不可逆胆碱酯酶抑制剂索曼的对抗作用。新霉素减低EPP量子含量,抑制MEPP幅度和减慢MEPP放电频率的浓度相应为0.03,0.1和0.32 mmol/L。链霉素抑制EPP和MEPP相应比新霉素强50和30倍。不影响量子含量的阈下剂量的新霉素(0.015mmol/L)和链霉素(0.8 mmol/L)能部分预防梭曼减少量子含量的作用。再增加此两药的浓度不能提高它们对抗梭曼的效用.同样,不影响MEPP频率的阈下剂量的新霉素和链霉素能完全预防梭曼加快MEPP频率的作用。认为新霉素和链霉素对神经肌接头抑制作用的主要作用部位是突触前递质诱发释放系统。其机理可能是它们竞争性地减少梭曼引起的向突触前膜内Ca~(2+)内流的增加。它们预防梭曼增加MEPP频率的机理也可能是如此。
The effects of aminoglycoside antibiotics neomycin and streptomycin on endplate potential (EPP) and microendothelial potential (MEPP) and inhibition of irreversible cholinesterase inhibition were observed on isolated rat diaphragm specimens with uneven traction Agent Soman’s antagonistic effect. The concentrations of neomycin that reduced the EPP quantum content, inhibited the MEPP amplitude and slowed the MEPP discharge frequency were 0.03, 0.1, and 0.32 mmol / L, respectively. Streptomycin inhibited EPP and MEPP correspondingly 50 and 30 times stronger than neomycin. Subliminal doses of neomycin (0.015 mmol / L) and streptomycin (0.8 mmol / L), which do not affect the quantum content, partially prevent soman from reducing the quantum content. Increasing the concentrations of these two drugs did not improve their effectiveness against soman.Moreover, subthreshold doses of neomycin and streptomycin, which did not affect the MEPP frequency, completely prevented soman from accelerating the MEPP frequency. It is believed that the main site of neomycin and streptomycin inhibition of neuromuscular junction is the presynaptic neurotransmitter release system. The mechanism may be that they competitively reduce soman-induced increases in pre-synaptic Ca2 + influx. The same may be true for their mechanism to prevent Soman from increasing the MEPP frequency.