Forshaw P J
Eur J Pharmacol. 1977 Apr 21;42(4):371-7. doi: 10.1016/0014-2999(77)90171-6.
Cadmium (0.125-1 mM) was found to inhibit the isometric response of the isolated rat hemidiaphragm during indirect stimulation, but not during direct stimulation. This effect of cadmium (1 mM) was completely reversed by ethyleneglycol bis-(aminoethyl)-N,N,N',N'-tetra-acetic acid (2 mM) or by L-cysteine (2 mM) but only partially by increased calcium. Cadmium (10 micronM) significantly reduced the quantal release of transmitter in the isolated phrenic diaphragm and a concentration of 0.1 mM frequently caused a complete failure of the endplate response after 30 min. The effect of cadmium on neuromuscular transmission could not be readily reversed by washing with cadmium-free solution. Miniature endplate potential frequency and amplitude were not significantly affected by cadmium (0.1 or 0.5 mM). The results suggest that the effect of cadmium on the isolated phrenic nerve-diaphragm is due largely to inhibition of calcium function at presynaptic nerve terminals.
研究发现，镉（0.125 - 1 mM）在间接刺激过程中可抑制离体大鼠半膈的等长反应，但在直接刺激时则无此作用。镉（1 mM）的这种作用可被乙二醇双（氨基乙基）-N,N,N',N'-四乙酸（2 mM）或L-半胱氨酸（2 mM）完全逆转，而增加钙浓度只能部分逆转。镉（10 μM）可显著降低离体膈神经膈肌标本中递质的量子释放，0.1 mM的镉浓度在30分钟后常导致终板反应完全消失。用无镉溶液冲洗并不能轻易逆转镉对神经肌肉传递的影响。微小终板电位的频率和幅度不受镉（0.1或0.5 mM）的显著影响。结果表明，镉对离体膈神经-膈肌的作用主要是由于其抑制了突触前神经末梢的钙功能。
