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作 者:黄勇华[1] 张微微[1] 郝小淑[1] 王伟[2] 王军[3] 谢荣堂[4]
机构地区:[1]北京军区总医院神经内科,北京100700 [2]北京军区司令部门诊部,北京100041 [3]北京军区总医院医务部,北京100700 [4]中国人民解放军264医院,山西太原030001
出 处:《中华老年心脑血管病杂志》2000年第3期200-202,共3页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基 金:国家自然科学基金!资助项目 ( 3 9770 75 3 )
摘 要:目的 探讨Ca2 + 与脑出血继发性损伤的关系及其尼莫地平的保护作用。方法 通过脑内注射胶原酶建立大鼠脑出血模型 ,采用草酸 焦锑酸钾电镜细胞化学技术 ,从形态学角度在观察脑出血后血肿周围脑组织超微病理变化的同时 ,直观地了解钙在缺血神经组织的分布 ,并观察Ca2 + 拮抗剂的保护作用。结果 脑出血组神经细胞、胶质细胞及毛细血管的超微结构有肿胀表现 ,细胞内可见多量Ca2 + 颗粒。钙拮抗剂治疗组细胞病理变化显著减轻 ,钙分布明显减少。对照组偶见Ca2 + 颗粒。结论 血肿周围组织存在水肿和继发性缺血 ,细胞内Ca2 + 稳态失调在神经细胞损害中起重要作用。Objective To investigate whether edema formation and ischemic injury surrounding hematoma is related to calcium overloading.Methods A model of collagenase induced intracerebral hemorrhage was used.The subcellular distribution of calcium in rat brain tissue surrounding the hematoma and the protective effects of calcium antagonists were evaluated with combined oxalate pyroantimonate electronmicroscopic cytochemical technique.Results There was regional accumulation of calcium in rat brain tissue surrounding the hematoma in intracerebral hemorrhage (ICH) group and the ultrastructural damage in brain tissue correlated strongly with the regional accumulation of calcium.Pretreatment with calcium antagonists (nimodipine for the voltage operated channel) resulted in less ultrastructural brain tissue damage and reduction of regional accumulation of calcium.Conclusions The results suggest that calcium overloading may play an important role in the process of cell death in rat brain tissue surrounding ICH and it is possible to reduce ICH injury through use of calcium antagonists.
分 类 号:R743.34[医药卫生—神经病学与精神病学]
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