Studies On Leukocyte Adhesion CD11b/CD18,Platelet CD61 And Pathological Change In Carbon Monoxide Poisoning Rat

Background Carbon monoxide poisoning is a common cause of poisoning disease in modern life, which is harmful to health and life. Especially "carbon monoxide poisoning delayed neuropsychologic sequelae" has became the focus to study,because it is difficult to predict and cure. It has been reported that a lot of hypothesis took part in carbon monoxide poisoning,such as ischemic-hypoxia,cell toxic injury,free radical formation,excitatory amino acids formation,apoptosis mechanism and so on. Among the total inflammatory mechanism has been studied during carbon monoxide poisoning in recent years. Researchers had observed that cytokines released generously, which can develop facilitating inflammation and thrombus, at the same time pathological findings observe that it is typical ischemic degeneration, flood silting up, vessel blunting, micro-thrombosis forming in cortex and hippocampus, leukocytes infiltrating around focus. Because leukocyte adhesion molecule CD11b/CD18,platelet CD61 can specificially reflect the condition of leukocyte and platelet, we may supply some evidence to evaluate status of inflammtion and thrombus in carbon monoxide poisoning.Object The project is on the basis of carbon monoxide poisoning model of rat, to observe leukocyte adhesion molecule CD11b/CD18,platelet CD61 on the dynamic state and brain pathological change at the just time, the aid is to probe into the mechanism of inflammation and platelet function in carbon monoxide poisoning, at last provide theorical foundation to anti-inflammation, anti-thrombus in carbon monoxide poisoning.Material and method 60 health, male rats, were divided into control group and operated group(1st 5, 3st 5, 7st 5, 15th 5, 30th 5, 60th 5). Carbon monoxide poisoning model of rat was established with injecting 99.9%CO into abdominal cavity, as compared, the control group was injected by atmosphere. At the just time, blood was obtained by orbital artery and vein to measure the concentration of COHb, and utilize flow cytometry and single-colonial technology to identify leukocyte adhesion molecule CD11b/CD18,platelet CD61, at the same time, prepare pathological slice.Results:1.Compared with the control group, the expression of leukocyte adhesion molecule CD11b/CD18 in experimental group was elevated generously, and keep in high level until 15th day.2.Compared with the control group, the expression of platelet CD61 in experimental group was elevated generously, and keep in high level until 30th day.3.Brain pathological change: there are some convertions in cortex of experimental groups: part of neuron cell took on ischemic degeneration in 1st, 3st , 7st , 15th , 30th day; the interval of cells increased, edemane of blood source,and scattered leukocyte infiltration.Conclusion:1.The research evidenced that inflammation and thrombus formation mechanism was related with carbon monoxide poisoning.2.The expression of CD11b/CD18 in experimental group was elevated generously,and induce leukocyte-endothelium adhesion. CD11b/CD18 may be regarded as a sensitive index to predict inflammation. 3.The expression of platelet CD61 in experimental group was elevated generously, Which indicates platelet activated. CD61 may be regarded as a sensitive index, and offer clue to forecast carbon monoxide poisoning delayed neuropsychologic sequelae.4.The research would provide the theory basis of anti-inflammation, anti-thrombus in carbon monoxide poisoning.