期刊文献+

亚低温治疗对重型颅脑损伤患者预后及其脑脊液中Aβ水平的影响 被引量:8

Influence of moderate hypothermia on cerebrospinal fluid amyloid β peptide level and prognosis in severe traumatic brain injury patients
下载PDF
导出
摘要 目的观察亚低温治疗对重型颅脑损伤(sTBI)患者预后及其脑脊液(CSF)中β淀粉样蛋白(Aβ)水平的影响,并探讨其意义。方法将60例sTBI随机分为观察组和对照组各30例,观察组采用亚低温治疗,对照组采用常温治疗;采用双抗体夹心ELISA法检测治疗前及治疗后第1、3、5、7天患者CSF中的Aβ,3个月后行GOS评定预后。结果对照组CSF中的Aβ水平逐渐升高,而观察组Aβ水平逐渐降低;治疗后3、5、7 d,两组AB水平比较,P均<0.01。治疗后3个月观察组GOS为(4.3±0.4)分,对照组为(2.2±0.2)分,两组比较,P<0.05。结论亚低温治疗可明显改善sTBI患者的预后,可能与其降低患者CSF中的Aβ水平有关。 Objective To study the effects of moderate hypothermia on cerebrospinal fluid amyloid 13 (Aβ) peptide level and prognosis in severe traumatic brain injury (sTBI) patients. Methods 60 sTB1 patients were randomly divided into observe group and control group,30 cases each. Patient in observe group were treated with moderate hypothermia. Aβ in cerebrospinal fluid was detected by ELISA at 1,3,5,7 days, and prognosis were evaluated by GOS. Results Aβ in cerebrospinal fluid increased time-dependent in control group ,but decreased time-dependent in observe group. GOS scroll was 4.3 ± 0.4 in observe group, and 2.2 ± 0.2 in control group ( P 〈 0.05 ). Conclusion Moderate hypothermia can inhabite the expression of Aβ and improve the clinical prognosis.
出处 《山东医药》 CAS 北大核心 2011年第2期1-2,共2页 Shandong Medical Journal
基金 天津市科委重点攻关项目(06yfszsf01200) 武警医学院院级重点资助项目(wyz201002)
关键词 重型颅脑损伤 亚低温疗法 脑脊液 Β淀粉样蛋白 brain injuries moderate hypothermia cerebrospinal fluid amyloid β peptide
  • 相关文献

参考文献11

  • 1Diller KR, Zhu L. Hypothermia Therapy for Brain Injury[J]. Annu Rev Biomed ,2009,11 (7) : 135-162.
  • 2Zhao H, Sapolsky RM, Steinberg GK. Interrupting repeffusion as a stroke therapy: ischemic postcondifioning reduces infarct size after focal ischemia in rats[J].Cereb Blood Flow Metab,2006,26 (9) : 1114-1121.
  • 3Kraus MF, Susmaras T, Caughlin BP, et al. White matter integrity and cognition in chronic traumatic brain injury: a diffusion tensor imaging study[ J]. Brain ,2007,130(10) :2508-2519.
  • 4Yah SD,Chen X,Fu J,et al. RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease [ J ]. Nature, 1996,82 (6593) :685 - 691.
  • 5Du YS, Zhu H, Fu J, et al. Amyloid-beta peptide-receptor for advanced glycation endproduct interaction elicits neuronal expression of macrophage-eolony stimulating factor: a proinflammatory pathway in Alzheimer disease [ J ]. Proc Nail Acad Sci USA, 1997,94 (10) : 5296-5301.
  • 6Webster S, Bonnell B, Rogers J. Charge-based binding of complement component C1 q to the Alzheimer amyloid beta-peptide [ J ]. Am Pathol, 1997,150 ( 5 ) : 1531-1536.
  • 7Said SI, Raza S, Erisha HI. Enhancement of systemic and pulmonary vasoconstriction by beta-amyloid peptides and its suppression by vasoactive intestinal peptide [J]. Ann NY Acad Sci, 1998,865 (7) :582-585.
  • 8Brody DL, Magnoni S, Schwetye KE, et al. Amyloid-b dynamics correlate with neurological status in the Injured human brain[ J]. Science,2008,321 ( 29 ) : 1221.
  • 9Loane DJ, Pocivavsek A, Moussa CEH, et al. Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury[ J]. Nature Meal,2009,15(4) :377.
  • 10Sai Z,Zhen L. A study of significance of continuous monitoring of jugular venous oxygen saturation and the effect of mild hypothermia in patients with severe traumatic brain injury [ J ]. Neurotrauma, 2006,23(5) :798.

同被引文献46

引证文献8

二级引证文献52

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部