摘要
目的:探讨蛋白激酶C(PKC)信号传导系统在气管平滑肌张力调节中的作用及氯胺酮、咪唑安定对其的影响。方法:研究不同浓度的PKC激动剂PMA(3×10-7~3×10-5mol/L)对静息状态下气管平滑肌张力的影响;研究两种浓度的PMA(3×10-6,3×10-5mol/L)及特异性PKC阻滞剂H-7(3×10-5mol/L)对乙酰胆碱(10-4mol/L)诱发气管平滑肌收缩力的调节作用及H-7、氯胺酮、咪唑安定对PMA效应的抑制作用。结果:3×10-7~3×10-5mol/L的PMA对静息状态下的气管平滑肌张力无明显影响,3×10-6mol/L的PMA可明显增强乙酰胆碱诱发张力的峰值和平台值,然而3×10-5mol/L的PMA并不能进一步增加乙酰胆碱的作用,张力平台值有所下降;3×10-5mol/L的H-7可完全抵消3×10-6mol/L的PMA效应。10-3mol/L氯胺酮和10-4mol/L咪唑安定和H-7有相似的效果。结论:PKC信号传导系统的激活并不能单独诱发离体气管平滑肌的收缩,但可使乙酰胆碱的收缩效应增加,氯胺酮和咪唑安定对PKC信号传导系统有抑制作用。
Objective:To investigate the role of protein kinase C ( PKC)signal pathway in the regulation of tracheal smooth muscle (TSM) tone and th e effect of ketamine and midazolam on the PKC signal pathway. Methods: By measuring the tones of isolated rabbit TSM, the direct action of different co ncentrations of PKC-specific activator PMA (3×10-7~3×10-5 mol/L) were observed. The effect of two different concentrations of PKC-specific acti vator PMA, inhibitor H-7 and ketamine, midazolam on regulation of contraction in isolated rabbit TSM induced by 10-4 mol/L acetylcholine (ACH) were studie d. Results:3×10-7~3×10-5 mol/L PMA had no effect on the TSM tone; but 3×10-6mol/L PMA could significantly enhanced the contracti on induced by ACH, 3×10-5 mol/L PMA could not further enhance the tension s; 3×10-5 mol/L H-7 could all countervail the effect of 3×10+{-6} mo l/L PMA; 10+{-3} mol/L ketamine and 10-4 mol/L midazolam had the simila r ef fect as H-7. Conclusion:The activation of PKC signal pathway could no t alone induce the contraction of isolated rabbit TSM but could enhance the acti on of ACH; ketamine and midazolam may inhibit the PKC signal pathway.
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
北大核心
2002年第2期125-127,共3页
Journal of Nanjing Medical University(Natural Sciences)
基金
南京医科大学科研基金资助项目(801MA9923)