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在颅内出血病人中,氧合血红蛋白(OxyHb)引起自由基、内皮素释放,脂质过氧化物产生,血管和周围神经损害以及内皮依赖性松驰因子抑制;破坏了血管的舒张与收缩平衡,引起脑血管的痉挛。其中内皮素(ET)除强大、持久的血管收缩作用外,还具有离子运输、神经传递、下丘脑—垂体功能调节、花生四稀酸生成和基因调控等作用。OxyHb与一氧化氮(NO)有极高的亲和力和促进ET的表达和释放,构成了脑内出血病人血管痉挛主要的病理基础。
In patients with intracranial hemorrhage, oxyhemoglobin (OxyHb) causes free radicals, endothelin release, lipid peroxides, vascular and peripheral nerve damage, and endothelium-dependent relaxation factor inhibition; disrupts the diastolic and contractile balance of blood vessels, Cause cerebral vasospasm. Endothelin (ET) in addition to a strong, long-lasting vasoconstriction, but also has ion transport, neurotransmission, hypothalamic-pituitary function regulation, arachidonic acid generation and gene regulation role. OxyHb and nitric oxide (NO) have very high affinity and promote the expression and release of ET, forming the main pathological basis of cerebral vasospasm in patients with intracerebral hemorrhage.