期刊文献+

犬颅脑火器伤后细胞内钙变化的实验观察 被引量:1

Experimental study of intracellular calcium change after craniocerebral fire-arm wounds in canines
暂未订购
导出
摘要 目的 探讨犬颅脑火器伤后脑细胞内Ca2 + 变化的规律 .方法 建立犬脑枪弹伤致伤模型后 ,制备脑组织的活细胞悬液进行原代培养 ;应用特异性钙离子荧光指示剂Fluo 3 AM标记 ,在激光扫描共聚焦显微镜下检测伤后不同时期、不同部位脑细胞内钙离子的分布情况 .结果 培养得到了贴壁的犬颅脑火器伤后的脑组织活细胞 .并观察到 30min后细胞内Ca2 + 即开始升高 (P <0 .0 5 ) ,72h达到高峰 (P <0 .0 1) ,78h后又呈下降的趋势 (P <0 .0 5 ) ;而挫伤区和震荡区的差别不大(P >0 .0 5 ) .结论 颅脑火器伤后细胞内Ca2 + 的增加 ,在伤后的不同时期和不同部位的分布具有时空规律性 ,这可能是火器伤后脑水肿和一系列继发性脑损害的原因之一 . AIM To study the regularity of intracellular Ca 2+ change after craniocerebral fire arm wounds in canines. METHODS After the canine craniocerebral missile wounds models were established, the living cells suspension liquids of the cerebral tissues were cultured. Intracellular Ca 2+ distribution was measured by calcium fluorescent probes Fluo 3/AM under laser confocal microscope at different periods and different positions of the canine brains . RESULTS The living cells of the cerebral tissues were cultured successfully after craniocerebral missile wounds. It was found that intracellular Ca 2+ increased obviously within 30 min( P <0.05), reached the summit at 72 h( P < 0.01 ),and then descended after 78 h( P <0.05).But the distinctions were unobvious between the regions of brain contusion and brain concussion .CONCLUSION The distribution of intracellular Ca 2+ demonstrated regularity at different periods,and at different positions of the brain.The changes of intracellular Ca 2+ was likely to be a pathophysiologic reason for the traumatic hydrocephalus and secondary lesion after craniocerebral fire arm wounds.
出处 《第四军医大学学报》 北大核心 2002年第23期2149-2151,共3页 Journal of the Fourth Military Medical University
基金 全军"九五"医学科研基金重点资助项目 (99 Z 1 4 6)
关键词 颅脑火器伤 细胞内 实验观察 激光共聚焦显微镜 钙离子 craniocerebral fire arm wound disease models ,animal laser confocal microscope calciumions
  • 相关文献

参考文献3

二级参考文献27

  • 1董培青 胡小琴.大血管手术的脑保护.心血管麻醉及体外循环[M].北京:人民卫生出版社,1997.489-498.
  • 2[1]Carbonell WS,Maris DO,McCall T et al. Adaptation of the fluid percussion injury model to the mouse. J Neurotrauma,1998,15(3):217
  • 3[2]Dunn Meynell AA,Hassanain M,Levin BE . Norepinephrine and traumatic brain injury: a possible role in post-traumatic edema. Brain Res, 1998, 800(2): 245
  • 4[3]Zhang X, Liu WP, Yi ShY et al. Principles for managing penetrating craniocerebral in juries caused by firearm missiles. J Clin Neurosci, 1996,3(3):229
  • 5[4]Dearden NM. Mechanisms and prevention of secondary brain damage during intensive care. Clin Neuropathol, 1998, 17(4): 221
  • 6[5]Fei Zh, Zhang X, Yi ShY.Brain TXA2 and PGI2 levels related to diffuse brain injury with secondary insults. J Clin Neurosci,1999,6(4):306
  • 7[6]He XSh, Yi ShY, Zhang X et al. Diffuse axonal injury due to lateral head rotation in a rat model. J Neurosurg, 2000, 93(4): 626
  • 8[7]Ng I, Yeo TT, Tang WY et al. Apoptosis occurs after cerebral contusions in humans.J Neurosurg, 2000,46(4):949
  • 9[8]Hausmann EH, Berman NE, Wang YY et al. Selective chemokine mRNA expression following brain injury. Brain Res, 1998, 788(1-2): 49
  • 10[11]Czosnyka M, Smielewski P, Piechnik S et al. Hemodynamic characterization of intracranial pressure plateau waves in head-injury patients. J Neurosurg,1999,91(1): 11

共引文献28

同被引文献2

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