低血容量休克复合内毒素血症时血和组织髓过氧化物酶的变化

研究观察失血性休克复合内毒素血症时血和组织髓过氧化物酶的变化规律。将雄性wistar大白鼠随机分为对照组、缺血组、缺血再灌流组和缺血再灌流复合内毒素组。用改良的髓过氧化物酶 (MPO)测定方法 ,测定血、肺和小肠组织MPO及相关指标的变化。结果显示肺组织MPO活性从失血性休克末开始升高 ,致内毒素血症时出现峰值 ;小肠组织MPO的活性在失血再灌流后显著升高 ,但在失血性休克复合内毒素血症后显著降低 ;血MPO活性于失血性休克和失血再灌流后均无显著性变化 ,复合内毒素后显著降低。结果表明失血再灌流后肺组织PMN扣留、聚集显著增加 ,内毒素血症促进PMN在肺中的扣留 ,这些变化与PMN上CD11b和CD18表达上调有关 ,提示失血再灌注复合内毒素时组织细胞损伤与PMN的粘附、扣留、激活有关。

Changes of plasma and tissue myelopetoxidase activity in hypovolemic shock combined with endotoxin challenge

To investigate the changes of myeloperoxidase (MPO)activity in blood and tissue from rats induced by hemorrhage combined with endotoxin challenge. A rat model of endotoxemia wete reproduced by henorrhagic shock combined with endotoxin infusion. MPO activity in blood and tissue wete dctermined.The influence of venous plasma on the expression of CD11b and CD18 on PMN was measured by ELISA. Lungs MPO actirty were markedly increased at post reperfusion and got to peak level after hemorrhagic shock post reperfusion could stimulate up regulation of CD11b and CD18 on PMN. MPO activities were significantly increased in tissue during hypovolemic shock combined with endotoxin challenge.The results suggest that PMN aggregated and activated in tissues is one of the main causes leading to the damage of organs.