中文摘要：

目的了解延迟整流钾通道在水杨酸钠导致耳鸣的机制中所起的作用。方法利用全细胞膜片钳技术研究水杨酸钠对急性分离的大鼠颞皮层神经元延迟整流钾通道的影响。结果水杨酸钠能够抑制延迟整流钾通道电流（IK（DR））的幅度,而且此抑制作用具有浓度依赖性（0.1～10 mmol.L-1）。水杨酸钠抑制IK（DR）的半抑制浓度（IC50）值为2.13mmol.L-1。1 mmol.L-1水杨酸钠将IK（DR）的激活曲线向超极化方向移动14 mV,将失活曲线向超极化方向移动17mV,并将失活后恢复曲线的时间常数（τ）延长为加药前的171%。结论水杨酸钠以浓度依赖的方式抑制IK（DR）,而且影响IK（DR）的激活和失活动力学特征。水杨酸钠对IK（DR）的影响可能与水杨酸钠导致耳鸣的机制有关。

英文摘要：

Aim To understand what role the delayed rectifier potassium channels play in the mechanism of salicylate-induced tinnitus.Methods The effects of salicylate on the delayed rectifier potassium channels in freshly dissociated auditory cortex neurons of rats were studied,using the whole-cell voltage clamp method.Results Salicylate blocked the delayed rectifier potassium current（IK（DR）） in a concentration-dependent manner（0.1~1 mmol·L-1）.The half-inhibition concentration（IC50） values for the blocking action of salicylate on IK（DR） were 2.13 mmol·L-1.At a concentration of 1 mmol·L-1,salicylate significantly shifted the activation curve negatively by 14 mV,shifted inactivation curve of IK（DR） negatively by 17 mV,and delayed its time constant（τ） of recovery curve from inactivation to 171% of the value before salicylate application.Conclusion Salicylate inhibits IK（DR） in rat auditory cortex neurons and significantly affects the activation and inactivation kinetics of the delayed rectifier potassium channels,which could be related to the mechanism of salicylate-induced tinnitus.