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出 处:《神经疾病与精神卫生》2004年第6期424-426,429,共4页Journal of Neuroscience and Mental Health
摘 要: 目的 从血液流变学变化的特点来探讨不同种类脑梗死的发病机制异同,评价东菱克栓酶治疗急性脑梗死的作用机制。方法 对100例健康者和 124 例脑梗死患者行血液流变学检查,并观察东菱克栓酶对不同种类脑梗死患者血液流变学指标和神经功能缺损恢复的作用。结果 脑梗死患者全血黏度、红细胞聚集性和纤维蛋白原均增高,且主干支组高于深穿支组(P <0.05),血小板聚集性也明显增高,但后者高于前者(P <0.05)。东菱克栓酶治疗后纤维蛋白原水平、红细胞聚集性、全血黏度和血小板聚集性较治疗前有显著性下降(P <0.05)。治疗后1周和1月,治疗组中主干支组、深穿支组的神经功能恢复均较对照组中的主干支组、深穿支组好 (P < 0.01)。结论 脑叶大梗死和脑深部小梗死在发病机制上有所不同。东菱克栓酶治疗上述两类急性脑梗死疗效肯定。Objective To probe the differences of pathogenic mechanism in the patients with different kinds of cerebral infarct, and to appreciate the pharmacological mechanism, clinical efficacy and security of Batroxobin. Methods Hemorheological parameters were measured in 100 healthy person and 124 patients with cerebral infarct. The effects of Batroxobin on hemorrheologyical parameters and neurological function defect of different cerebral infarct patients were observed. Results Before therapy hemorheological parameters were higher in the patients than in the normal persons. Blood viscosity, erythrocyte aggregability and plasma fibrinogen levels in the group with the cerebral infarcts due to alterations in major blood vessels or cortical branch than those with central branch infarct (P<0.05 or P<0.01)). However, plaque aggregability in the latter was higher than in the frontier (P<0.05). Plasma fibrinogen levels, erythrocyte aggregability and blood viscosity in the therapy group was significantly lower after treatment. The recovery of neurological functions in therapy group was better than the controls (P<0.01). Conclusions With regard to pathogenic mechanism, the difference was found between the cerebral infarcts due to alterations in major blood vessels or cortical branch and the central branch infarct. The therapy efficacy of Batroxobin was certain.
关 键 词:血液流变学 脑梗死 东菱克栓酶 药物治疗 纤维蛋白原
分 类 号:R743[医药卫生—神经病学与精神病学]
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