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Objective@#oevaluateclinical curative effect of oxiracetam injection in the treatment of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) .@*Methods@#Methods 52 patients with DEACMP were randomly divided into the observation group and the control group, 27 cases in the observation group and 25 cases in the control group. The 2 groups were adopted the treatment to improve the cerebral microcirculation and other symptomatic, the observation group on the basis of treatment for the treatment of oxiracetam Injection. Quantitative electroencephalogram (QEEG) and event-related potential P300 were used to evaluate the therapeutic effects of the 2 groups before and after treatment.@*Results@#After treatment, QEEG value and event related potential P300 in observation group were decreased with statistically significant, respectively (P<0.05) , compared with the control group after treatment, the observation group excepted the occipital lobe, left parietal lobe, left around central and other indicators, QEEG and P300 oflatent period was shortened while the bank widens with statistical significance (P<0.05) .@*Conclusion@#Olathe injection of DEACMP patients recovery have certain curative effect.
ABSTRACT
Objective To observe the effect of erythropoietin(EPO)in rats with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods A total of 90 male adult SD rats were randomly divided into three groups:blank control group(BC group),air control group(AC group)and DEACMP group. Time points(1,3,7,14,21 and 28 days after acute carbon monoxide poisoning)were set for measuring the changes. Pure CO were injected into the abdominal cavity of the rats from DEACMP group for several times to estab-lish DEACMP model. Rats in AC group were injected with equal volume of air by the same way. BC group were without any treatment. Morris water maze test was used to measure the cognitive behavior. The apoptosis of pyrami-dal neurons at hippocampus was measured by TUNEL. The expression of erythropoietin(EPO)in hippocampus was measured by immunohistochemistry. Results The average escaped latency of rats in DEACMP group increased after poisoning compared with rats in other two groups(P<0.05). The apoptosis of pyramidal neurons in hippocam-pus increased from day 1 after the CO poisoning. It reached the peak at day 7 and it still had a high expression at day 28. The apoptotic index in DEACMP group increased significantly compare with that of BC group and AC group (P < 0.05). The expression of EPO in hippocampus was found increased from day 1 after the CO poisoning and reached the peak at day 3. It began to reduce at day 7. The expression in DEACMP group was higher than those of other two groups (P < 0.05). Conclusions It may be one of the causes of the DEACMP that the expression of EPO decreased in the middle and late stage after CO poisoning and its anti-apoptosis was decreased.
ABSTRACT
Objective To observe the effect of erythropoietin(EPO)in rats with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods A total of 90 male adult SD rats were randomly divided into three groups:blank control group(BC group),air control group(AC group)and DEACMP group. Time points(1,3,7,14,21 and 28 days after acute carbon monoxide poisoning)were set for measuring the changes. Pure CO were injected into the abdominal cavity of the rats from DEACMP group for several times to estab-lish DEACMP model. Rats in AC group were injected with equal volume of air by the same way. BC group were without any treatment. Morris water maze test was used to measure the cognitive behavior. The apoptosis of pyrami-dal neurons at hippocampus was measured by TUNEL. The expression of erythropoietin(EPO)in hippocampus was measured by immunohistochemistry. Results The average escaped latency of rats in DEACMP group increased after poisoning compared with rats in other two groups(P<0.05). The apoptosis of pyramidal neurons in hippocam-pus increased from day 1 after the CO poisoning. It reached the peak at day 7 and it still had a high expression at day 28. The apoptotic index in DEACMP group increased significantly compare with that of BC group and AC group (P < 0.05). The expression of EPO in hippocampus was found increased from day 1 after the CO poisoning and reached the peak at day 3. It began to reduce at day 7. The expression in DEACMP group was higher than those of other two groups (P < 0.05). Conclusions It may be one of the causes of the DEACMP that the expression of EPO decreased in the middle and late stage after CO poisoning and its anti-apoptosis was decreased.
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Objective:To investigate the levels of AP-1 in hippocampus of rats at different time points after carbon monoxide poisoning.Methods: Carbon monoxide poisoning delayed encephalopathy model by using intraperitoneal injection of carbon monoxide.Uesd HE observed the pathological changes in hippocampus of rats.The levels of AP-1 was observed by immunohistochemistry and Western blot analysis.TUNEL was used to detect apoptotic neurons in hippocampal CA1 area.Results: HE dyeing conditions,the hippocampus cell of air group (AC) and blank group (BC) were normal at each time point.Pathological changes occurred in the hippocampus cell of Carbon monoxide group (CO),reduction in the number of cells,disorder of cells,intercellular space expansion,nuclear fragmentation,anachromasis and pyknotic.Immunohistochemical results,the AP-1 expression level at each time point in group CO were higher than group AC and BC.On 3th day it reached a peak.The comparison at all time points among the groups in the first three days were significantly different in statistics(P<0.05).Western blot results,the expression of AP-1 was consistented with the immunohistochemical results on the time distribution trend.TUNEL results,AI in group CO was higher than those in group AC and BC at all time points,there were significant differences(P<0.05) and 7th reached the peak of apopotsis.Conclusion: Inside the hippocampus of rats,there are increasing in AP-1 . Maybe it is one of the important pathogenesis of DEACMP .