一氧化氮在八肽胆囊收缩素抗脂多糖致离体兔胸主动脉低血管反应性中的作用  

Role of nitric oxide in the inhibition of lipopolysaccharide-induced thoracic aortic hyporeactivity by cholecystokinin in vitro

作　　者：李淑瑾[1] 凌亦凌[1] 王殿华[1] 谷振勇[1] 孟爱宏[1] 朱铁年[1] 

机构地区：[1]河北医科大学病理生理学教研室,河北石家庄050017

出　　处：《中国病理生理杂志》2002年第7期770-773,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助课题 (No .395 70 304) ;河北省自然科学基金资助课题 (No.3974 31)

摘　　要：目的 :探讨一氧化氮 (NO)在八肽胆囊收缩素 (CCK - 8)减轻脂多糖 (LPS)致离体兔胸主动脉收缩反应降低中的作用。方法 :用LPS、LPS +CCK或溶剂孵育离体兔胸主动脉环 14h ,检测其对苯肾上腺素 (PE)的收缩反应 ,及PE预收缩后对NO合酶 (NOS)底物L -精氨酸的反应 ;用NOS抑制剂氨基胍 (AG)或Nω-硝基 -L -精氨酸 (L -NNA)预孵育后胸主动脉环对PE收缩反应的变化 ,并检测胸主动脉NOS活性。结果 :LPS孵育胸主动脉环 14h ,导致其对PE的收缩反应明显降低 ,NOS活性明显增高 ;同时加入CCK - 8则明显提高胸主动脉环对PE的收缩反应 ,程度与AG一致 ,且抑制LPS诱导的NOS活性。结论 :CCK - 8减轻LPS致离体兔胸主动脉收缩反应降低的作用与抑制NOS活性、减少NO生成有关。AIM: To investigate the effect of cholecystokinin octapeptide(CCK-8) on the L-arginine-nitric oxide(NO) pathway in rabbit thoracic aortae treated with lipopolysaccharide(LPS). METHODS: The isolated thoracic aortic rings(TARs) from rabbits were incubated with LPS, LPS+CCK or vehicle for 14 h. Then the contractility to phenylephrine(PE) by TARs and the response to L-arginine(L-Arg) by pre-contractile TARs were measured. In addition, we added NO synthase(NOS) inhibitors aminoguanidine(AG)and N ω-nitro-L-arginine(L-NNA) into organ baths to observe the changes of vascular contractility to PE. NOS activity in isolated TARs were also detected. RESULTS: Incubation of TARs with LPS for 14 h resulted in an increase of NOS activity and a reduction of contractility to PE. Treatment with CCK-8 significantly inhibited the increased NOS activity in thoracic aortae and improved the hypocontractility of TARs to the same degree as AG. CONCLUSION: CCK-8 may improve the hypocontractility of TARs induced by LPS by inhibiting the activity of NOS.

关 键 词：缩胆囊素 胆多糖类 胸主动脉 一氧化氮 血管收缩反应 低血压 

分 类 号：R331.33[医药卫生—人体生理学]