出血性休克大鼠脑组织NF-κB的表达

Hemorrhagic shock and NF-κB expression in rat cerebral tissue

目的:通过观察脑组织中核因子-κB(NF-κB)活性的变化,探讨出血性休克与脑缺血损伤的关系。方法:将SD大鼠随机分成5组,对照组(sham组)、休克组、全部自体血复苏组、3倍出血量的复方氯化钠液(林格液)复苏组、2倍出血量的林格液加1/2出血量的自体血复苏组。采用大鼠股动脉放血休克模型,休克1h。分别于股动脉、股静脉插管后,休克后和不同液体复苏30min后取脑组织。常规病理形态学检查,观察脑水肿和炎性细胞浸润的程度;免疫组化方法检测脑组织NF-κB的表达。结果:与sham组比较,休克组、各复苏组脑组织中NF-κB表达均明显增加(P<0.01),并可见不同程度的脑水肿和炎性细胞浸润;但3倍出血量的林格液复苏和2倍出血量的林格液加1/2出血量的自体血复苏后,脑组织中NF-κB的表达增加明显低于全部自体血复苏组(P<0.05或P<0.01),脑水肿和炎性细胞浸润亦较轻。结论:出血性休克(出血量达总血量35%,维持60min)可通过炎性级联反应使脑组织中NF-κB激活,引起脑缺血损伤。3倍出血量的林格液或2倍出血量的林格液加1/2出血量的自体血复苏,使脑组织NF-κB的表达增加明显减少,可能对减轻脑缺血损伤有益。

Objectives To investigate the relation between hemorrhagic shock and cerebral isehemie injury by observing nuclear factor kappa-B （NF-κB） expression in rat cerebral tissue. Methods Sprague-Dawley rats were randomly divided into sham group, hemorrhagic shock group （HS）, and resuscitated groups including whole blood return group （WBR）, Ringer＇s solution （RS） at 3x shed blood volume （SBV） （3R）, RS at 2x SBV plus blood return at 1/2x SBV （2R）. Hemorrhagic shock was induced by intermittently withdrawing blood from a femoral catheter. All rats except those in sham or HS group were then resuscitated with different liquids. The extent of brain edema and infiltration of inflammatory cells was observed; NF-κB expression in the rat cerebral tissue was detected by using immunohistochemistry. Results Compared with that in sham group, NF-κB expression in HS and resuscitated groups was significantly increased with various extents of brain edema and infiltration of inflammatory cells （P 〈 0.01） . NF-κB expression in 3R or 2R group was markedly decreased as compared with that in WBR group （ P 〈 0. 05 or P 〈 0.01） . Conclusion NF-κB-triggered inflammatory cascade becomes early activated during hemorrhagic shock （acute blood loss was 35% of the estimated total blood volume over a period of 60 min）, resuhing in cerebral ischemic injury. Resuscitation with RS at 3x SBV or 2x SBV plus blood return 1/2x SBV can decrease NF-κB expression and may be value of cerebral ischemic injury induced by hemorrhagic shock.