哌替啶的舒血管作用及其机制  

Mechanisms of pethidine-induced vasodilatation

作　　者：张雄[1] 柴灵莺[2] 童晓嵋[2] 陆源[1] 夏强[1] 

机构地区：[1]浙江大学医学院基础医学部,浙江杭州310031 [2]浙江大学医学院

出　　处：《浙江大学学报（医学版）》2004年第2期166-169,共4页Journal of Zhejiang University(Medical Sciences)

基　　金：浙江省自然科学基金青年人才专项基金 (RC990 38)资助项目

摘　　要：目的 :探讨哌替啶扩张血管导致低血压的机制。方法 :制备大鼠离体主动脉环 ,记录血管环张力 ,观察哌替啶对高钾和苯肾上腺素 (Ph E)预收缩血管的作用。结果 :哌替啶不影响血管的静止张力 ,但可对高钾和 Ph E诱导的收缩产生非内皮依赖的舒张作用 ,并呈剂量 -反应关系。哌替啶既不影响咖啡因诱导的血管收缩 ,也不改变钌红作用后对高钾诱导收缩的抑制作用。在无钙条件下 ,哌替啶仍能抑制 Ph E的收缩 ,也抑制后续加入钙后引发的收缩。结论 :哌替啶对高钾和 Ph E诱导的血管收缩有舒张作用 ,机制可能与其阻断细胞膜钙通道和抑制 IP3敏感钙池的钙释放有关。Objective: To investigate the vasodilating effects of pethidine, particularly in association with intracellular calcium. Methods: Aorta rings of Sprague-Dawley rats, with or without endothelium, were prepared in organ bath to measure the vascular tone. Pre-contractions by KCl (80 mmol/L) and phenylephrine (PhE) (10 -6 mol/L) were induced. Results: Pethidine did not alter the resting tension of aorta rings, but produced dose-dependent relaxation in KCl and PhE pre-treated aorta rings with or without endothelium. Pethidine did not change the caffeine-stimulated contraction, and still had similar inhibition in KCl pre-contracted aorta rings after pretreatment with ruthenium red. Pethidine decreased the contractile responses induced by PhE in Ca 2+-free solution or by adding calcium into Ca 2+-free solution. Conclusion: Pethidine could produce an endothelium-independent vasodilatation in KCl and PhE pre-contracted aorta rings, which is related to inhibition of Ca 2+ entry and IP3-sensitive Ca 2+ release in vascular smooth muscle.

关 键 词：哌替啶/药理学 血管/药物作用 IP3受体 RYANODINE受体 主动脉 

分 类 号：R965[医药卫生—药理学]