创伤性休克大鼠中性粒细胞CD18和糖皮质激素受体的变化及纳络酮的治疗作用

Expression of neutrophil CD18,glucocorticoid receptor and therapeutic effects of naloxone during traumatic shock in rats

目的：探讨中性粒细胞粘附分子ＣＤ１８（ＰＭＮＣＤ１８）和中性粒细胞糖皮质激素受体（ＰＭＮＧＲ）在大鼠创伤性休克早期的动态变化及盐酸纳络酮的治疗作用。方法：采取软组织损伤加颈动脉放血作为大鼠创伤性休克动物模型，分别于创伤前、休克后４５、９０、２１０、３３０和４５０分钟取血，测定各组大鼠的ＰＭＮＣＤ１８和ＰＭＮＧＲ含量。复苏组和纳络酮组则于休克后９０分钟开始实施复苏措施。结果：休克组休克４５分钟ＰＭＮＣＤ１８表达值明显增高，随后逐渐下降，至休克后４５０分钟与基础表达值仍相差非常显著（Ｐ＜０．０１）；ＰＭＮＧＲ随休克时间的延长逐渐下降；复苏１２０分钟后上述改变最为显著。肝、肺组织切片发现，复苏组复苏后１２０分钟毛细血管内有大量白细胞粘附于血管内壁，同时血管周围有白细胞浸润，组织细胞浊肿，复苏３６０分钟后上述改变减轻。纳络酮治疗组复苏后１２０、２４０和３６０分钟ＰＭＮＣＤ１８较复苏组同时间点的结果明显降低（Ｐ均＜０．０１），ＰＭＮＧＲ较复苏组同时间点的结果明显升高（Ｐ均＜０．０１）；肝、肺组织学检查显示，纳络酮治疗组复苏后毛细血管内白细胞附壁较复苏组同时间点明显减少。结论：创伤性休克及复苏时，ＰＭＮ与内皮细胞粘附明?

Objective :To investigate changes in neutrophil CD18 (PMN CD18) and glucocorticoid receptor (PMN GR) and protective effects of naloxone (NLX) after early traumatic shock in rats. Methods :Traumatic shock was induced by soft tissue injury plus hemorrhage of carotid artery.Systemic blood was collected at pre shock,45,90,210,330 and 450 minutes after shock,respectively.PMN CD18 and PMN GR levels were measured at various intervals.Resuscitation was performed at 90 minutes following shock in both resuscitation and NLX groups. Results :PMN CD18 increased markedly during traumatic shock,especially at 45 minutes,then decreased gradually,but remained higher than that of control group at 450 minutes after shock (P<001);PMN GR decreased gradually along with prolongation of shock;peaking at 120 minutes after resuscitation.Tissue examination showed that a lot of leukocytes adhered to liver and lung capillary in resuscitation group at 120 minutes after resuscitation,meanwhile,the cells surrounding capillary show the above changes decreased at 360 minutes after resuscitation.PMN CD18 reduced dramatically in NLX group compared with resuscitation group at corresponding intervals (all P<001),while PMN GR sites increased in NLX group (all P<001);tissue examination showed that there were less leukocytes adhered to liver and lung capillary after resuscitation in NLX group than that of resuscitation group. Conclusions :The adhesion of PMN endothelial cell is significantly increased during traumatic shock,and it may be due to the upregulation of PMN CD18 expression.The upregulation of PMN CD18 expression may be due to the downregulation of PMND2GR,NLX can provide protective effects by inhibiting the expression of PMN CD18 and increasing the PMN GR sites.