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甲强龙对出血性休克大白鼠的影响
引用本文:王钢,杨晓临,崔泽实,关福兰.甲强龙对出血性休克大白鼠的影响[J].中国现代医学杂志,2005,15(3):343-348.
作者姓名:王钢  杨晓临  崔泽实  关福兰
作者单位:1. 中国医科大学附属第一医院,急诊科,辽宁,沈阳,110001
2. 中国医科大学基础医学院,辽宁,沈阳,110001
3. 中国医科大学实验技术中心,辽宁,沈阳,110001
摘    要:目的研究甲强龙(甲泼尼龙)对出血性休克大白鼠的影响并探讨其机制.方法大白鼠经动脉放血,造成失血性休克模型,随后用自体血和生理盐水从静脉回输,进行复苏.复苏前大白鼠随机分成三组假休克组,休克组和甲强龙治疗组.结果复苏后72 h,休克组的生存率降至20%,而甲强龙治疗组的生存率达80%,差异显著(P<0.01).复苏后18h器官病理取材,H-E染色,光镜下显示休克组大白鼠的心、肺、肾、肝组织出现不同程度水肿、细胞变性、间质炎性细胞浸润等.甲强龙治疗组大白鼠的上述脏器的病理改变明显减轻.复苏后18 h,CK、Cr、ALT、AST、ALKP检测,休克组明显升高,而甲强龙治疗组只有轻度增高,差异非常显著(P<0.01).复苏后2 h,肝脏枯否细胞用LPS刺激后,休克组的细胞内Ca2+浓度和TNF-α产量明显增高,而甲强龙治疗组轻度增高,差异显著(P<0.01).结论甲强龙可以通过抑制kupffer细胞内Ca2+升高和激活,阻止TNF-α的过度产生,降低机体系统性炎症反应程度,最终减轻出血性休克大白鼠脏器的损伤和降低死亡率.

关 键 词:甲强龙  出血性休克  大白鼠  治疗组  复苏后  增高  轻度  减轻  差异  程度

Effect of methylprednisolone on hemorrhagic shock in rats
WANG Gang,YANG Xiao-lin,CUI Ze-shi,GUAN Fu-lan.Effect of methylprednisolone on hemorrhagic shock in rats[J].China Journal of Modern Medicine,2005,15(3):343-348.
Authors:WANG Gang  YANG Xiao-lin  CUI Ze-shi  GUAN Fu-lan
Affiliation:WANG Gang1,YANG Xiao-lin2,CUI Ze-shi3,GUAN Fu-lan2
Abstract:Objective: To investigate the effect of methylprednisolone (MP) on hemorrhagic shock in rats and elucidate the underlying mechanisms. Method: Wistar rats were bled to induce the shock and subsequently resuscitated with shed blood and normal saline. Just prior to resuscitation, the rats were divided into three groups: sham group, shock group and shock+MP groups. Results: 72 h after resuscitation, the survival rate of shock group decreased to 20%, while the survival rate of shock+MP group was 80%, the difference was significant (P <0.01). 18 h after resuscitation, pathologic alterations of organs showed: in shock group, pulmonary edema, leukocyte infiltration in interstitial tissue and cellular degeneration occurred. MP reduced these pathological alterations significantly. 18 h after resuscitation, creatine phosphokinase, transaminases and creatinin were elevated significantly in shock group,while these in shock+MP group were elevated slightly, the differences were significant (P <0.01). Increases in intracellular calcium and production of TNF-α by isolated kupffer cells stimulated by endotoxin were elevated significantly by hemorrhagic shock, which were totally prevented by MP (P <0.01). Conclusion: Methylprednisolone reduces organ injury and mortality caused by hemorrhagic shock by blocking increase of intracellular calcium, activation and production of TNF-α of kupffer cells and preventing systemic progressive inflammation responses.
Keywords:hemorrhagic shock  methylprednisolone  kupffer cell  intracellular calcium  TNF-α
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