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作 者:廖鑫鑫[1] 黄胜[1] 杨华中[2] 黄琼瑶[3] 彭飞[3] 刘年猛[3] 孙慧[3]
机构地区:[1]湖南师范大学医学院 [2]湖南师范大学医学院药理学教研室 [3]湖南师范大学医学院寄生虫学教研室,湖南长沙410006
出 处:《湖南师范大学学报(医学版)》2010年第1期11-13,21,共4页Journal of Hunan Normal University(Medical Sciences)
基 金:国家大学生创新项目资助课题(081054240);湖南省教育厅资助课题(06c501)
摘 要:目的:研究血水草生物碱(Eomecon chionantha Hance alkaloids,ECA)对钉螺足跖平滑肌收缩活动的影响及与毒蕈碱型乙酰胆碱受体(muscarinic acetylcholine receptors,mAChR)的关系,探讨其减低钉螺附壁上爬、增强灭螺效果的作用机制。方法:采用离体钉螺足跖平滑肌实验方法,观察ECA对钉螺足跖平滑肌收缩活动的影响。结果:5.0、10.0、20.0 mg/L ECA均可增加钉螺足跖平滑肌张力、减小收缩幅度、加快收缩频率;2×10-6mol/L阿托品可明显降低由ECA所至的钉螺足跖平滑肌的张力,而对其所至的收缩幅度及收缩频率影响不明显;6×10-6mol/L阿托品则可显著地拮抗ECA引起的钉螺足跖平滑肌兴奋作用,使钉螺足跖平滑肌的张力及收缩幅度均明显降低,但对其所至收缩频率影响不明显。结论:ECA能兴奋钉螺足跖平滑肌;ECA引起的钉螺足跖平滑肌兴奋作用部分由mAChR介导,其作用机制可能与激活受体依赖性钙通道(receptor operated calcium channel,ROCC)有关。Objecti ve To investigate the relationship between the muscarinic acetylcholine receptors(mAChR) and the effects of Eomecon chionantha Hance alkaloids(ECA) on the contraction of Oncomelania foot smooth muscles,and to explore the mechanism of ECA in decreasing the snail climbing adhesion and increasing snail-killing.Methods The in vitro experiment of isolated foot smooth muscles of Oncomelania was used in the study to observe the effects of ECA on the foot smooth muscles of Oncomelania.Results ECA 5.0,10.0 or 20.0 mg / L enhanced observably the resting tension,decreased the contraction range and increased the contraction frequency of Oncomelania foot smooth muscles;Atropine 2 ×10-6mol/L depressed observably the tension of oncomelania foot smooth muscles induced by ACE,but it had not marked influence on the contraction range and the contraction frequency of oncomelania foot smooth muscles;The excitations induced by ECA on the foot smooth muscles of Oncomelania were observably inhibited by 6×10-6mol/L atropine,reducing the tension and the contraction range of Oncomelania foot smooth muscles induced by ACE,but it had not marked influence on the contraction frequency of oncomelania foot smooth muscles.Conclusion ACE had an excitatory effect on the foot smooth muscles of oncomelania,which was partially mediated via muscarinic acetylcholine receptors (mAChR),and this mechanism is likely to related with activing receptor operated calcium channel(ROCC).
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