皮层下动脉硬化性脑病患者外周血红细胞和血小板内钙离子含量的变化
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Changes of IECa2+ in Blood Erythrocyte and Platelet in Patients with Binswager’s Disease
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    摘要:

    研究Binswager病患者外周血血细胞内钙离子浓度,探讨钙离子异常分布与Binswager病形成的关系,并寻找预防措施。Binswager病患者2 6例,健康对照者2 0例,采用流式细胞术检测外周血血细胞内钙离子浓度。结果发现,Binswager病组血细胞内钙离子浓度显著高于对照组(P<0 .0 5 )。重度脑萎缩组钙离子含量高于轻中度脑萎缩组。智能检查评分结果发现,痴呆组血细胞钙离子增加较正常组及痴呆前期组明显(P<0 .0 5 )。结果提示,Binswager病形成机制与钙离子浓度分布异常有关。钙离子分布异常可能激活细胞内源性核酶和T淋巴细胞受体的交联诱发突触传递中神经递质释放,使红细胞变形能力和血小板聚集性改变,加重脑组织缺血、缺氧程度。应用钙拮抗剂可预防因脑循环障碍所致的Binswager病。

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    Aim To discuss the relationship of abnormal distribution of Ca 2+ and formation of 26 Binswager’s disease, and to find how to prevent the disease. Method Binswager group and control group were detected by flow cytometry. Results IECa 2+ in blood hemocytes was significantly higher in encephalatrophy group than that in control group (p<0.05). In the group with severe cerebral atrophy manifested by computer tomography, IECa 2+ was higher than that of mild and moderate cerebral atrophy group. In the group with dementia, which were detected by the score of intelligent determination, the increase of IECa 2+ was much more remarkable than that of control group and prophase dementia group (p<0.05). Conclusions The formation mechanism of Binswager’s disease was related to abnormal distribution of IECa 2+. The abnormal distribution of IECa 2+ may activate cross-linking of cellular endogenic ribozyme and antibody of T lymphocyte, evoke neurotransmitter release in synapses, change the deformation ability of erythrocyte and aggregation function of platelet, thereby aggravate ischemia of cerebral tissues. Calcium antagonists can prevent Binswager’s disease caused by cerebral circulation disorder.

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薛慎伍,张兆岩,李玮.皮层下动脉硬化性脑病患者外周血红细胞和血小板内钙离子含量的变化[J].中国动脉硬化杂志,2004,12(6):713~715.

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  • 收稿日期:2004-03-18
  • 最后修改日期:2004-08-10
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