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作 者:张艳丽[1] 王晓丽[1] 吴会蔚[1] 李超[1] 孙丽华[1] 霍荣[1] 杨宝峰[1] 王玲[1,2]
机构地区:[1]哈尔滨医科大学药理学教研室,黑龙江省生物医药重点实验室国家重点实验室培育基地,黑龙江哈尔滨150081 [2]哈尔滨医科大学生理学教研室,黑龙江哈尔滨150081
出 处:《哈尔滨医科大学学报》2010年第1期45-48,52,共5页Journal of Harbin Medical University
基 金:黑龙江省教育厅资助项目(11521081);黑龙江省博士后启动基金资助项目
摘 要:目的观察脑缺血所致心脏损害,血浆及心肌局部血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)的变化及卡托普利对其的影响,探讨脑心综合征的发病机制。方法用线栓法栓塞右侧大脑中动脉建立脑心综合征模型,检测心电图,电镜下观察心肌细胞的亚显微结构,放射免疫法测定血浆和心肌局部AngⅡ的含量。结果电镜结果显示大鼠脑缺血后心肌细胞有明显损伤;放射免疫结果显示脑缺血2h血浆和心肌局部AngⅡ水平均高于假手术组(P<0.01);在给予卡托普利后心肌损伤减轻,AngⅡ含量降低。结论脑缺血可以引起明显的心肌损伤,肾素-血管紧张素系统(RAS)可能参与脑心综合征的发生发展。Objective To investigate the pathological damages of myocardium,the alterations of angiotensin Ⅱ in plasma and myocardium as well as the effects of captopril on acute focal cerebral ischemic rats;to further probe the mechanism of arrhythmia in cerebro-cardiac syndrome model rats.Methods The cerebro-cardiac syndrome model rats were induced by occluding right middle cerebral artery and the ECG was monitored.The microstructure of the myocardium was examined by electronic microscope.Plasma and myocardial angiotensin Ⅱ levels were determined using radioimmunoassay(RIA).Results Damages of myocardial tissue were obviously after cerebral ischemia,and those damages were attenuated in captoril groups.Angiotensin Ⅱ levels in plasma and myocardium were increased in cerebral ischemia groups compared with sham group(P0.01),and decreased in captopril groups compared with ischemia group.Conclusion Acute focal cerebral ischemia could lead to myocardial damages.Renin-angiotensin system(RAS) may play an important role in the development of myocardial damages induced by cerebral ischemia.
分 类 号:R743.3[医药卫生—神经病学与精神病学] R-332[医药卫生—临床医学]
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