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作 者:刘晓燕[1] 郭霞珍[1] 李立华[1] 杨云霜[1]
机构地区:[1]北京中医药大学基础医学院
出 处:《中医杂志》2012年第6期507-509,512,共4页Journal of Traditional Chinese Medicine
基 金:北京市自然科学基金资助项目(7072038)
摘 要:目的研究寒邪导致高血压大鼠发生脑卒中的机制。方法将100只SD大鼠随机分为正常组(30只),模型组(40只),假手术组(30只)。每组于降温前、降温中、降温后3个时间点取材,采用双肾双夹法复制易卒中型肾血管性高血压模型。通过人工模拟气温的骤降诱发脑卒中,检测各组大鼠内皮素-1(ET-1)、血管紧张素Ⅱ(AngⅡ)、精氨酸血管加压素(AVP)、一氧化氮(NO)水平的变化。结果降温后模型组大鼠20只,发生脑出血的有13只(其中10只存活,3只死亡),7只无明显变化。其他组均无脑卒中发生。气温骤降使正常组大鼠AngⅡ和AVP水平上升,而NO水平明显下降(P<0.05)。模型组大鼠在气温骤降的刺激下血ET-1、AngⅡ和AVP(P<0.05)水平均上升,但NO水平与正常组大鼠相反,不降反升。降温后模型组大鼠NO、AngⅡ、AVP水平较降温前升高,ET-1水平则较降温前和同时间点的正常组下降(P<0.05)。结论气温骤降促进了高血压大鼠血管舒缩反应性的紊乱,可能是寒邪促发高血压状态脑卒中发病的重要机制。Objective To study the mechanism of stroke in hyper te nsive rats induced by cold pathogens.Methods Totally 100 SD rats were ra ndomized into normal group(n=30),model group(n=40) and sham operation group( n=30).Reno vascular hypertension model was established by clipping two sides of renal arter y.Stroke was induced by simulating a sudden drop in temperature.Ten rats were randomly selected before,during and after drop in temperature respectively in e a ch group.The level of endothelin-1(ET-1),angiotensinⅡ(AngⅡ),arginine va so pressin(AVP) and NO was detected in each group before and after sudden drop in temperature.Results After the sudden drop in temperatu re,13 rats suffered cere bral hemorrhage in 20 rats of the model group,among which 3 died.Stroke did no t attack in other groups.The levels of AngⅡ and AVP were increased in t he normal group,but the level of NO were significantly decreased(P0.05). The levels of ET-1,AngⅡ and AVP were significantly increased in the model gr oup( P0.05),and the level of NO was increased as well.The levels of NO,Ang Ⅱ,AVP and NO were increased in the model rats,while the level of ET-1 was significantly d ecreased as compared with that of the normal group at the same time(P0.0 5).Con clusion The mechanism of stroke in hypertensive rats induced by cold pa thogens is due to disorder of angiokinesis.
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