| Carbon monoxide ( CO) as a colourless and ordorless gas continues to be a common cause of poisoning mortality and morbidity worldwide. More than half death caused by poisoning event is related to carbon monoxide poisoning in many countries. Although the living condition has been improved, CO poisoning e-vents have not decreased correspondencely. More than a century of scientific investigation, the mechanisms of injury and methods of treating carbon monoxide poisoning are poorly understood. The target organs of CO are brain and heart mainly. After immediately treatment, 23 -47% of the victims would still suffer delayed neuropsychologic sequelae (DNS). The pathogenesis of and risk factor for DNS remain unknown . The patients have impairments of concentration, attention , language, learning , memory, or motor function or have depression, dementia or psychosis that develops between 2-28 days after poisoning. DNS may cause a series of problems such as loss of labor abilities, decrease of living quality and big cost for medical services. China has a high incidence of CO poisoning. According to a investigation in First Hospital of China Medical University , CO poisoning ranked the second position among poisoning diseases while its mortality ranked first position.The mechanism of neuropsychologic damage caused by CO is unknow by far. The study show after CO poisoning excess lipid hyperoxidation and neutro-phils adherance can be seen and expression of early immediate gene increased. Hyperbaric therapy has given to CO poisoning patients since 1960s. The effectiveness and indications for HBO therapy remain controversial.This research utilized a animal model to study the mechanism of brain damage after CO exposure. Apoptosis, release and elimination of free radicals, permeability of blood - brain barrier, ultrastrusture, as well as cytokines will be ob-served. HBO therapy group will provide the evidence of its effects.MethodsMice were divided into four groups that is control, CO poisoning, CO poisoning plus NBO and CO poisoning plus HBO. The parameters detected are as followings -.1. The establishement of CO poisoning model. Mice were put into the 5L chamber with which CO level is maintained in 2500 - SOOOppm. Mice were kept in the chamber till comatose.2. The expression of gene Bel -2, Bax, p53 and the percentage of apopto-sis cells of the brain after acute carbon - monoxide poisoning were detected by the flow cytometric method. The ultrastructure difference of the brain cells between the mice accepting and not - accepting HBO treatment after acute carbon monoxide poisoning was observed by H - 600 TEM, And the changes of blood -brain barrier permeability were determined by detection of EB content in mice brains with spectrophotometer.3. Measurement of cytokines Brain tissue was homogenized and centri-fuged. Proinflammation cytokines TNF -a, IL-1B, IL-8 and anti - inflammation cytokine IL - 10 of mice brain were measured using ELISA, as well as sereum level of TNF - a, ET and NO using radio - immunology.4. Measurement of NO,NOS, and MDA as well as SOD, GSH -Px, and CAT. Free radicals system NO, NOS, and MDA and anti - oxidation enzymes SOD, GSH - Px, and CAT were detected by spectrophotometer.Results1. The expression of gene Bcl -2,p53and Bax and ,the percentage of ap-optotic cells in brain elevated after acute carbon monoxide poisoning. The peak points were 1 hour, 3 days and 7 days respectively. Ultrastructure was changed after acute carbon monoxide poisoning, and the HBO therapy could eliminate thechange. The permeability of blood - brain barrier was increased after acute carbon monoxide poisoning and the protection could be achieved by the application of L - NAME 15 min before or 30 min after carbon monoxide exposure.2. The significant elevation of TNF - a, IL - 1B, and IL - 8 were found in CO exposure brain of mice. Anti - inflammation cytokine IL - 10 also increased in same group. Sereum level of TNF - a, ET and NO increased too. There were significantly...
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