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机构地区:[1]首都医科大学宣武医院药物研究室神经变性病教育部重点实验室,北京100053 [2]济宁医学院神经生物学研究所,山东济宁272067
出 处:《医学综述》2011年第20期3041-3043,共3页Medical Recapitulate
基 金:国家重点基础研究计划-973计划项目(2003CB517104);国家自然科学基金(90709011;30472184;30973513)
摘 要:高脂血症不仅可以导致大动脉形态和功能改变,还可以诱导微循环系统发生表型改变。这种变化主要表现为小动脉血管扩张受损、毛细血管灌流不足、小静脉黏附因子表达增加。内皮细胞、白细胞、血小板激活和免疫细胞源性细胞因子参与微循环系统对高脂血症的应答调节,表明高脂血症微循环系统的变化对大血管病变有显著影响。对高脂血症造成的微循环功能障碍和炎症进行早期干预,会有效降低缺血性疾病高致残率、致死率。Hypercholesterolemia is a recognized risk factor for coronary artery and cerebral vascular diseases because of its effects on large arterial vessels(atherosclerosis).However,there is a growing body of evidence that hypercholesterolemia also leads to microvascular dysfunction long before the appearance of atherosclerotic lesions in large vessels.The microvascular dysfunction induced by hypercholesterolemia is manifested in arterioles as impaired vasodilation and in postcapillary venules as an accumulation of rolling and adherent leukocytes as well as platelets,whereas both vascular segments(arterioles and venules)exhibit an oxidative stress.The activation of multiple cell types(endothelial cells,leukocytes,platelets)and involvement of different segments of the microcirculation suggest that circulating soluble mediators(eg,cytokines)and/or cell adhesion-dependent signaling contribute to the microvascular alterations of hypercholesterolemia.Targeting the microvascular inflammation and oxidative stress is a fascinating approach for novel therapies in order to decrease morbidity and mortality of chronic and acute diseases.
分 类 号:R331.3[医药卫生—人体生理学]
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