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目前,缺血性脑卒中急性期血液呈高凝状态已被证实,但对出血性脑卒中血液状态的研究较少。本文对脑内出血(ICH)急性期患者血液中凝血、抗凝及纤溶状态的研究现状作一综述。 一、脑组织损伤后血液凝血及纤溶的变化 凝血包括内、外源两条凝血途径。内源途径由接触因子ⅹⅡ接触血管内膜下胶原纤维而激发,外源途径由组织凝血活酶复合体所激发。脑组织中含有丰富的组织凝血活酶。1962年,Lewis等给狗静脉注射脑组织凝血活酶,证实能引起消耗性凝血病。1973年,
At present, the acute hypercoagulable state of blood in ischemic stroke has been confirmed, but there is little research on the blood state of hemorrhagic stroke. This article reviewed the research status of blood coagulation, anticoagulation and fibrinolysis in patients with acute intracerebral hemorrhage (ICH). First, changes in blood coagulation and fibrinolysis after brain tissue injury Coagulation, including both internal and external coagulation pathways. The endogenous pathway is triggered by exposure of the contact factor ⅹII to intima-derived collagen fibers, and the exogenous pathway is activated by the tissue thromboplastin complex. Brain tissue is rich in tissue thromboplastin. In 1962, Lewis and other intravenous injection of brain tissue thromboplastin to dogs, proved to cause consumptive coagulopathy. In 1973,