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应用蜗内电位(EP)、听神经动作电位(AP)同步记录技术观察了前列腺素(PGs)合成抑制剂消炎痛对于速尿耳蜗毒性的影响。速尿加消炎痛组EP(mV)和AP_(N1)相对振幅(％)下降程度均低于单纯速尿组,电位恢复速率则明显大于速尿组。实验提示速尿对耳蜗靶组织血管纹的损伤与PGs介导有关。消炎痛对抗速尿的作用机理可能在于抑制了耳蜗内源性PGs的生物合成,因而减轻了速尿对EP及AP_(N1)的抑制效应。
The effects of indomethacin, a prostaglandin (PGs) synthesis inhibitor, on furosemide cochlea toxicity were observed by simultaneous recording of intraciliary potential (EP) and auditory nerve action potential (AP). The decrease of relative amplitude (%) of EP (mV) and AP_ (N1) between furosemide and indomethacin group was lower than that of pure furosemide group and the recovery rate of potentials was significantly higher than furosemide group. Experimental results suggest that furosemide has a protective effect on the stria vascularis of the target tissue. The mechanism of action of indomethacin against furosemide may be that the biosynthesis of endogenous PGs in the cochlea is inhibited, thereby reducing the inhibitory effect of furosemide on EP and AP_ (N1).