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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] 贺颖[2]
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 [2]北京军区总医院内分泌科,北京100700
出 处:《中国病理生理杂志》2001年第11期1060-1063,共4页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目 (No .395 70 30 4) ;河北省自然科学基金资助项目 (No .397431)
摘 要:目的和方法 :应用离体血管环张力测定技术 ,观察八肽胆囊收缩素 (CCK - 8)对脂多糖 (LPS)诱导兔离体胸主动脉反应性变化的影响。在扫描电镜下观察内皮细胞超微结构的变化 ,以探讨CCK - 8抗内毒素休克作用的可能机制。结果 :LPS(10 0mg/L)孵育后的胸主动脉环对乙酰胆碱 (ACh )的内皮依赖性舒张反应降低 ,且呈时间依赖性 ;对苯肾上腺素 (PE)的收缩反应降低 ;孵育 7h血管内皮细胞结构损伤 ;CCK - 8(1mg/L)可减轻LPS的损伤效应 ;CCK - 8(1mg/L)单独孵育对胸主动脉的舒缩反应及内皮细胞的超微结构无明显影响。结论 :CCK - 8能减轻LPS诱导兔离体胸主动脉反应性的异常改变 ,这可能是CCK - 8抗内毒素休克作用的机制之一。AIM and METHODS: To elucidate the mechanism of anti-endotoxic shock of cholecystokinin octapeptide(CCK-8), the effects of CCK-8 on changes in rabbit thoracic aortic reactivities induced by lipopolysaccharides(LPS) in vitro were studied, and the ultrastructure of the endothelial cells was observed under scanning electron microscope. RESULTS: Incubation of thoracic aortic rings(TARs) with LPS(100 mg/L) resulted in an time-dependent impairment of the endothelium-dependent relaxations to acetylcholine(incubation for 3, 7, 14 h), a reduction of contractive response to phenylphrine(incubation for 14 h) and ultrastructural injury in endothelial cells(incubation for 7 h), all of which were alleviated by concomitant incubation with CCK-8(1 mg/L). In contrast, neither the vascular contractions nor the relaxations were affected by CCK-8 (1 mg/L) alone. CONCLUSION: CCK-8 improved the vascular reactivities in the presence of LPS, which may be one of the anti-endotoxic shock mechanisms of CCK.
关 键 词:缩胆囊素 脂多糖类 胸主动脉 血管内皮 八肽胆囊收缩素 兔 离体血管环张力测定
分 类 号:R543[医药卫生—心血管疾病]
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