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目的 探讨中性粒细胞粘附分子ＣＤ１８（ＰＭＮＣＤ１８）、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洛酮（ＮＬＸ）的治疗作用。方法 动物模型采用软组织损伤加颈动脉放血法，分别采用流式细胞仪和放射配体结合法测定ＰＭＮＣＤ１８ 、ＰＭＮＧＲ 的表达值。结果 休克组休克４５ ｍｉｎＰＭＮＣＤ１８ 表达值明显增高，随后逐渐下降，但至休克７．５ ｈ 仍高于基础表达值，两者差异有非常显著性（ Ｐ＜０ ．０１） ；ＰＭＮＧＲ 随休克时间的延长逐渐下降，到复苏２ ｈ 后最显著。肝、肺组织切片发现，复苏后２ ｈ 毛细血管内有大量白细胞粘附于血管内壁，复苏后６ ｈ 减轻。治疗组复苏后２ ｈ 、４ ｈ、６ ｈ ＰＭＮＣＤ１８ 较复苏组同时相点的结果明显降低（ Ｐ＜ ０．０１） ，而ＰＭＮＧＲ 则明显升高（ Ｐ＜ ０ ．０１）；组织学检查显示治疗组复苏后毛细血管内白细胞附壁较复苏组同时相点明显减少。结论 创伤性休克及复苏时，中性粒细胞内皮细胞（ＰＭＮＥＣ）粘附明显增强，与ＰＭＮＣＤ１８ 的表达增加有关，ＰＭＮＧＲ的减数调节是ＰＭＮＣＤ１８ 表达增加的原因之一，纳洛酮（ＮＬＸ） 可通过增加ＰＭＮＧＲ 位点?
Objective To investigate the dynamic changes of neutrophil adhesion molecule CD18 (PMNCD18) and neutrophil glucocorticoid receptor (PMNGR) in the early stage of traumatic shock in rats and the treatment of naloxone hydrochloride (NLX) effect. Methods Animal models were induced by soft tissue injury and carotid artery bleeding, and the expressions of PMNCD18 and PMNGR were determined by flow cytometry and radioligand binding assay respectively. Results The expression of PMN-CD18 in shock group at 45 min was significantly increased, then decreased gradually, but it remained higher than the basal expression level at 7.5 h after shock, the difference between the two groups was significant (P <0.01) Shock duration decreased gradually, to 2 h after the most significant recovery. Liver and lung tissue sections showed that a large number of white blood cells adhered to the blood vessel wall within 2 hours after resuscitation and were relieved at 6 hours after resuscitation. The results of simultaneous phase point of PMNCD18 in resuscitation group were significantly lower at 2 h, 4 h and 6 h after resuscitation (P <0.01), while PMNGR was significantly higher (P <0.01) School tests showed that the treatment group after the recovery of capillaries within the capillary wall than the recovery group significantly reduced phase point. Conclusions During traumatic shock and resuscitation, the adhesion of neutrophil-endothelial cells (PMN-EC) was significantly increased, which was related to the increased expression of PMN-CD18. The down-regulation of PMN-GR was the reason for the increase of PMN-CD18 expression First, naloxone (NLX) by increasing PMN GR sites?