期刊文献+

大鼠窒息心脏骤停期间脑皮质β肾上腺素能受体和血中NO的变化 被引量:2

Changes of β-adrenoceptor in the cerebral cortex and blood nitric oxide during cardiac arrest in an asphyxiated rat model
下载PDF
导出
摘要 目的研究心脏停搏期间脑皮质β肾上腺素能受体(β受体)的变化,检测心脏停搏前后血液NO浓度变化,探讨其意义。方法采用放射性配基结合分析方法,检测大鼠在窒息心脏停搏期间脑皮质β受体的变化。采用化学发光法,检测动物心脏停搏前后血中NO浓度的变化。将动物随机分为正常对照(A),手术对照(B),窒息10min(C)、20min(D)和30min(E)5组,每组6只。结果β受体数量D和E组分别与A、B、C组比较,差异极其显著(P<0.01)。各组间受体亲和力无明显变化。C组血中NO浓度与A、B组比较,差异极其显著(P<0.01)。结论在窒息心脏骤停早期,脑皮质β受体数量无明显变化,随着心脏停搏时间延长,其数量明显增加。心脏停搏以后,与心脏停搏前比较,血中NO浓度明显升高。 Objective Changes of β-adrenoceptor(β-AR)in the cerebral cortex and blood nitric oxide (NO)during asphyxiated cardiac arrest were investigated.Methods The β-AR of the membrane fraction of the cerebral cortex was analyzed by radioligand binding assay with the use of [3H]-DHA. The NO concentration was detected by the luminol chemiluminescence.The rats were divided into control(A),sham(B),asphyxiated 10 min(C), 20 min(D) and 30 min(E)group.Results The β-AR number in the cerebral cortex was (37.15±2.74)fmol/mg pr,(39.09±1.46)fmol/mg pr,(49.67±4.98)fmol/mg pr,(81.62±10.37)fmol/mg pr and (83.50±9.22) fmol/mg pr in the group A,B,C,D and E respectively.The β-AR number in group D and E was greater than that of group A,B and C respectively (P<0.01).The affinity(KD) of β-AR in the cerebral cortex among the groups didn't change.The NO concentration in blood in the group C (2 044.01±291.23) nmol/L was greater than that of the group A(1 156.12±258.16)nmol/L and B(1 299.17±269.44) nmol/L respectively(P<0.01).Conclusion The β-AR number in the rat cerebral cortex increased(up-regulation)after cardiac arrest with the cardiac arrest time prolonged.The NO in the blood increased significantly after cardiac arrest.
出处 《中国急救医学》 CAS CSCD 北大核心 2005年第6期427-429,共3页 Chinese Journal of Critical Care Medicine
基金 国家863计划课题部分内容(No.2002AA2Z3321)
关键词 心脏骤停 Β肾上腺素能受体 一氧化氮 Heart arrest β-adrenergic receptor Nitric oxide(NO)
  • 相关文献

参考文献12

  • 1White BC,Sullivan JM, DeGracia Dj, et al.Brain ischemia and reperfusion: molecular mechanisms of neuronal injury[ J ] .J Neurol Sci,2000,179(S1 - 2) :1 - 33.
  • 2Monteiro P, Duarte AI, Moreno A, et al.Carvedilol improves energy production during acute global myocardial ischemia [ J ] .Euro J Pharmacol, 2003,482( 1 - 3) :245 - 253.
  • 3Hashiguchi A, Yano S, Morioka M, et al. Up - regulation of endothelial nitric oxide synthase via phosphatidylinositol 3 - kinase pathway contributes to ischemic tolerance in the CAI subfield of gerbil hipoocampus[ J ] .J Cereb Blood Flow Metab,2004,24(3) :271 - 279.
  • 4Mizuki T, Kobayashi H, Ueno S, et al. Differential changes in α- and β-adrenoceptors in the cerebral coryex and hippocampus of the mongolian gerbil after unilateral brain ischemia [ J ]. Stroke, 1995,26 ( 12 ) : 2333 - 2337.
  • 5Savitz SI, Erhardt JA, Anthony JV, et al.The novel β-blocker, carvedilol,provides neuroprotection in transient focal stroke[ J ] .J Cereb Blood Flow Metab,2000,20(8) : 1197 - 1204.
  • 6Junker V, Becker A, Huhne R, et al. Stimulation of β - adrenoceptors activates astrocytes and provides neuroprotection [ J ]. Euro J Pharmacol,2002,446(1 - 3):25 - 36.
  • 7Thiemennmm C, Szab 6 C, Mitchell JA, et al. Vascular hyporeactivity to vasoconstrictor agents and hemodynamic decompensation in hemorrhagic shock is mediated by nitric oxide[ J ] .Proc Natl Acad Sci USA, 1993,90(1):267 - 271.
  • 8Zhang ZG, Chopp M, Bailey F, et al. Nitric oxide changes in the tat brain after transient middle cerebral artery occlusion[ J ] .J Neurol Sci, 1995,128(1):22 - 27.
  • 9Gursoy - Ozdemir Y, Bolay H, Saribas O, et al. Role of endothelial nitric oxide generation and peroxynitite formation in reperfusion injury after focal cerebral ischemia[ J ]. Stroke, 2000,31 (8) : 1974 - 1981.
  • 10Castillo J, Rama R, Davalos A. Nitric oxide - related brain damage in acute ischemic stroke[ J ]. Stroke, 2000,31 (4) : 852 - 857.

同被引文献10

引证文献2

二级引证文献1

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