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.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
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)
