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作 者:鄂明艳[1] 刘金鑫 李振凤[3] 张奇[3] 綦海[3]
机构地区:[1]哈尔滨医科大学附属第三医院放疗科,150040 [2]大庆市第五医院心内科 [3]哈尔滨医科大学附属第二医院心内科教育部省部共建心肌缺血机理与诊疗技术重点实验室
出 处:《中国地方病学杂志》2010年第5期500-503,共4页Chinese Jouranl of Endemiology
基 金:教育部高校博士点专项科研基金(20060226014);黑龙江省杰出青年科学基金(JC-05-16)
摘 要:目的 通过冠状动脉内注射月桂酸钠,观察月桂酸钠对缺血性心肌冠状动脉微血管血栓形成和心肌形态学变化的影响.方法 雄性SD大鼠54只,体质量(250±30)g.将大鼠按体质量随机分为3组:月桂酸钠组、假手术组、对照组,每组18只.将大鼠开胸,分离腹主动脉,在夹闭腹主动脉的同时,月桂酸钠组向其根部注入月桂酸钠(1 mg/kg),在20 s后立即松夹;假手术组注入等体积生理盐水,对照组不做任何处理.每组分别于术后第1、7、28天处死4~6只大鼠,取心肌组织制成切片,经HE与马休黄-酸性品红-苯胺蓝染色,光镜下观察心肌冠状动脉微血管血栓形成及受损心肌的形态学变化,透射电镜下观察血管内皮细胞超微结构的变化.结果 月桂酸钠组大鼠心肌冠状动脉微血管中,可见多量由血小板纤维蛋和胶原构成的血栓;假手术组、对照组大鼠微血管中未见血栓形成.月桂酸钠组冠状动脉微血管内皮细胞超微结构较假手术组、对照组改变明显,细胞间紧密连接增宽,微血管挛缩狭窄.月桂酸钠组随时间延长心肌炎纤维化加重,假手术组、对照组未见明显变化.结论 心肌冠状动脉微血管血栓形成是月桂酸钠致缺血性心肌损伤的主要原因,内皮损伤可能是月桂酸钠导致冠状动脉微血管血栓形成的主要机制.Objective To observe the morphological changes of myocardium and intracoronary microthrombus by intracoronary injection of sodium laurate. Methods Fifty four male SD rats, weighing (250 ± 30)g,were randomly divided into 3 groups according to weight: sodium laurate group, sham group and control group,eighteen rats in each group. In sodium laurate group, exposed and occluded the aorta while injected with sodium laurate(1 mg/kg) for 20 seconds. In sham group, took normal saline instead and no operation in control group. At the 1st, 7th and 28th day after the operation, 4 - 6 rats were selected randomly from each group and euthanized. The cardiac tissue were obtained and fixed for pathological study. After HE staining and modified Lendrum staining,micro-thrombosis and morphological changes of injured myocardium were detected under light microscope. The ultrastructure change of vascular endothelial cells was observed with transmission electron microscopy (TEM).Results Microthrombus consisting of platelet fibers and collagen could be observed only in sodium laurate group.The ultrastroctural changes of endothelial cells were significant in sodium laurate group compared with other two groups. TEM analysis showed that tight junctions between cells became wide and microvascular became narrowed in sodium laurate group. The fibrosis changes were enhanced in sodium laurate group compared with sham group and control group with the time prolong. Conclusions Micro-thrombosis is one of mechanisms in the development of sodium laurate induced ischemic myocardial injury. Endothelial injury may be the mechanism for sodium laurate leading to microthrombus.
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