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蛛网膜下腔出血后脑血管痉挛的生物学标记物 被引量:6

Biological markers of cerebral vasospasm after subarachnoid hemorrhage
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摘要 脑血管痉挛是蛛网膜下腔出血(subarachnoid hemorrhage,SAH)最常见和最凶险的并发症,如果不能早期诊断和治疗,将会造成迟发性脑缺血和迟发性缺血性神经功能缺损,严重影响患者的转归。SAH会造成氧化应激和炎症反应,引发血管痉挛,进而导致脑组织损伤。很多研究显示,这些病理生理学过程中多种代谢产物浓度或活性会发生改变,明确这些标记物发生变化的部位、时间和趋势,对于探讨SAH后脑血管痉挛的发生机制和寻找更佳的治疗靶点具有重要临床意义。文章对SAH后脑血管痉挛的生物学标记物进行了综述。 Cerebral vasospasm is the most common and most dangerous complication of subarachnoid hemorrhage (SAH). If it can not be diagnosed and treated early, it will result in delayed cerebral ischemia and delayed ischemic neurological deficits, and seriously affect the outcomes of patients. SAH can cause oxidative stress and inflammation, causing vasospasm, and leading to brain tissue damage. Numerous studies have shown that the concentrations and activities of numerous metabolites will change in these pathological physiological processes. Identification of the changes of location, time and trend of these markers has important clinical significance for investigating the mechanism of cerebral vasospasm after SAH and seeldag better therapeutic targets. This article reviews the molecular markers of cerebral vasospasm after SAH.
作者 吕涛 张晓华
出处 《国际脑血管病杂志》 2015年第6期469-473,共5页 International Journal of Cerebrovascular Diseases
基金 国家自然科学基金
关键词 蛛网膜下腔出血 血管痉挛 颅内 生物学标记 Subarachnoid Hemorrhage Vasospasm, Intracranial Biological Markers
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  • 1Becker KJ. Epidemiology and clinical presentation of aneurysmal subarachnoid hemorrhage[ J]. Neurosurg Clin N Am, 1998, 9: 435-444.
  • 2Longstreth WT Jr, Nelson LM, Koepsell TD, et al. Clinical course of spontaneous subarachnoid hemorrhage: a population- based study in King County, Washington[ J ]. Neurology, 1993, 43: 712-718.
  • 3Rodriguez Garcia PL, Rodr[guez Pupo LR, Rodriguez Garcia D. Diagnosis of delayed cerebral ischaemia and cerebral vasospasm in subarachnoid haemorrhage E J ]. Neurologia, 2010, 25: 322- 330.
  • 4Chen LC, Hsu C, Chiueh CC, et al. Ferrous citrate up-regulates the NOS2 through nuclear transloeation of NFKB induced by free radicals generation in mouse cerebral endothelial cells [ J ] PLoS One, 2012, 7: e46239.
  • 5Munakata A, Ohkuma H, Shimamura N. Effect of a free radical scavenger, edaravone, on free radical reactions: related signal transduction and cerebral vasospasm in the rabbit subarachnoid hemorrhage model[ J ]. Aeta Neuroehir Suppl, 2011, 110: 17-22.
  • 6Luo C, Yi B, Chen Z, et al. PKGItx inhabits the proliferation of cerebral arterial smooth muscle cellinduced by oxyhemoglobin after subarachnoid hemorrhage[ J ]. Aeta Neurochir Suppl, 2011, 110: 167-171.
  • 7Link TE, Murakami K, Beem-MiUer M, et al. Oxyhemoglobin- induced expression of R-type Ca2 + channels in cerebral arteries. Stroke, 2008, 39: 2122-2128.
  • 8Ohnlshi H, Iabara K, Kaku Y, et al. Haptoglobin phenotype predicts cerebral vasospasm and clinical deterioration after aneurysmal subarachnoid hemorrhage[J]. J Stroke Cerebrovasc Dis, 2013, 22: 520-526.
  • 9Sehba FA, Mostafa G, Friedrich V Jr, et al. Acute microvascular platelet aggregation after subarachnoid hemorrhage[ J ]. J Neurosurg, 2005, 102: 1094-1100.
  • 10Frstermann U1, Mtinzel T. Endothelial nitric oxide synthase in vascular disease: from marvel to menace[ J]. Circulation, 2006, 113 : 1708-1714.

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