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作 者:李培武[1,2] 王先坤[2] 种晓琴[3] 李培杰[2] 崔鸿斌[2] 鲁彦[4] 傅仲学[1]
机构地区:[1]重庆医科大学附属第一医院普外科,重庆400030 [2]兰州大学第二医院急诊科 [3]解放军第一医院高压氧神经内科 [4]解放军第一医院检验科
出 处:《中国临床药理学与治疗学》2013年第7期754-759,共6页Chinese Journal of Clinical Pharmacology and Therapeutics
基 金:甘肃省技术研究与开发专项计划项目(0709TCYA062)
摘 要:目的:观察内皮素-1(1-31)[ET-1(1-31)]在大鼠孤束核(Nucleus tracts solitarius,NTS)产生的心血管效应,并探讨其作用机制。方法:雄性SD大鼠90只,其中50只随机分为双侧NTS注射组、单侧NTS注射组和人工脑脊液(aCSF)组,分别在双侧或单侧NTS微量注射ET-1(1-31)(0.5~2.0pmoL)或aCSF(100nL),观察ET-1(1-31)在NTS内的心血管效应。11只大鼠观察ET-1(1-31)(1.0pmoL)在NTS水平对动脉压力反射功能(BRS)产生的影响。其余29只大鼠分别预先给予ETA受体拮抗剂BQ123、ETB受体拮抗剂BQ788、非选择性谷氨酸受体拮抗剂犬尿烯酸(KYN)或对照(aCSF),探讨ET-1(1-31)在大鼠NTS内产生的心血管效应机制。结果:在大鼠NTS双侧或单侧微量注射ET-1(1-31)剂量依赖性降低大鼠血压并减缓心率;NTS双侧微注射ET-1(1-31)(1pmoL)显著减弱大鼠BRS(P<0.05);ETA受体拮抗剂BQ123或KYN显著减弱单侧NTS微量注射ET-1(1-31)(1.0pmoL)产生的降低血压和减缓心率作用(P<0.05);单侧NTS注射ETB受体拮抗剂BQ788对NTS微量注射ET-1(1-31)(1.0pmoL)产生的降低血压和减缓心率作用没有显著的影响(P>0.05)。结论:NTS微量注射ET-1(1-31)能够降低麻醉大鼠的血压并减缓心率,其作用可能是由ETA受体和谷氨酸受体所介导。Objective: To observe the cardiovascular functions of endothelin-1(1-31)[ ET-1(1-31)] within the nucleus tract solitarius(nucleus tracts solitarius, NTS) and explore their mechanism. Methods: 90 male SD rats were included into the present study. Among them, 50 were randomized into bilateral or unilateral microinjection of ET-1(1-31)(0.5~2.0 pmol)or aCSF (100 nl) group, in which ET-1(1-31) (0.5~2.0 pmol) or aCSF (100 nl) was bilaterally or unilaterally applied to observe the dose-dependant responses of ET-1(1-31) within the NTS. ET-1(1-31) (1.0 pmol) or aCSF (100 nl) was bilaterally applied into the NTS to observe the influences of ET-1(1-31) (1.0 pmol) on the arterial baroreflex function (BRS) within the bilateral NTS in 11 rats. ETA receptor antagonist BQ123, ETB receptor antagonist BQ788 or non-selective glutamate receptor antagonist kynurenine (KYN) was prior applied to explore the mechanism of ET-1(1-31) within the NTS in 29 rats. Results: Bilateral or unilateral microinjection of ET-1(1-31) into the NTS produced dose-dependant hypotension and bradycardia of rats.Bilateral microinjection of ET-1(1-31) into the NTS significantly decreased the BRS function. Pretreatment with BQ123 or KYN significantly decreased BP and HR responses induced by unilateral microinjection of ET-1(1-31) (1.0 pmol) into the NTS. Conclusion: ET-1(1-31) within the NTS produces hypotension and bradycardia, mediated by ETA receptors and glutamate receptor at least partly.
关 键 词:内皮素-1(1-31) 孤束核 心血管 压力反射
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