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Background:Carbon monoxide(CO)is a colorless, odorless,bland and common asphyxial gas in our life.The population of the carbon monoxide poisoning and the dead after acute carbon monoxide poisoning lists the first place among various kinds of acute poisoning in our country. Most of patients can resume through right and effective therapy after carbon monoxide poisoning.But a part of patients who are serious comatose may reappear“delayed encephalopathy”after a“false recover period”,which often includes amnesia,mood disorder,consciousness,extrapyramid disorder and so on.The pathogenesis of delayed encephalopathy in acute carbon monoxide poisoning(DEACMP) still remains unclear.Nowadays,thare are some hypothesis.It has been reported that some hypothesis were likely to took part in DEACMP,such as ischemic/hypoxia,microthrombus, apoptosis, excitatory glutamate toxity,peroxidation,et al.CO poisoning mainly lead to brain hypoxia,which can cause vascular endothelial cell swelling and further brain dysaemia,which cause the cerebral thrombosis,and focal ischemic necrosis of the cerebral cortex and basal ganglia at last.CO poisoning may increase excitatory glutamate releasing significantly, which is concerned with neurotoxicity is mediated by CO poisoning and delayed neuronal death.In addition,some researchers found that apoptosis reached the max at the 7th day after acute CO poisoning.Opioid receptors are members of the G-protein-coupled receptor superfamily,which includeκ、δ、μand orphanin receptors.There areκl、κ2、κ3 three subtybes inκpioid receptor,μl andμ2 two subtybes inμpioid receptor,δ1 andδ2 two subtybes inδpioid receptor.They are widespread in the central nervous system.Recently,some researchers discovered thatδandκopioid receptor could protect neurons in the ischemic/hypoxia circumstances and make they survival.Up-regulation of theδopioid receptor expression increased survivability of the neurons to ischemic/hypoxia stress,andδreceptor could prevent apoptosis and could reduce neuronal damage was induce by hypoxia and excitatory glutamate when it was activated.Besides,κopioid receptor is also considered to prevent excitatory glutamate releasing significantly and lighten brain injury.Theμreceptors may be relevant to mood disorder.Object:The project is on the basis of carbon monoxide poisoning model of rat,to observe changes of opioid receptors after acute carbon monoxide poisoning,to explore the role of the opioid receptors against hypoxia and ischemia and if DEACMP can be interfered and prevented by the opioid receptors.Method:90 healthy male rats,were divided into control group and operated group(6thhour,1stday ,2th day,3thday,4thday,7thday,14thday,21stday,28thday group,5rats in every group).The rat model of acute carbon monoxide poisoning was built by carbon monoxide peritoneum injection,to detect the changes of opioid receptors of frontal lobe,Striatum and hippocampus of control group and experimental group in RT-PCR. Statistical differences between experimental group and control group were analyzed by using two independent samples t test.Results:1.The rats were convulsive,restless,then stationary,paralytic after carbon monoxide poisoning.2.Compared with the control group,δopioid receptor level of the experimental group was elevated in frontal lobe,striatum and hippocampus of rats of acute carbon monoxide poisoning.From the 7th day to 28th day,theδreceptor level rose generously.3.Compared with the control group,κopioid receptor level of the experimental group was overall elevated in frontal lobe,striatum and hippocampus of rats of acute carbon monoxide poisoning.From the 7th day to 28th day,theκreceptor level rose generously.4.Theμopioid receptor level was not changed approximately in frontal lobe,striatum and hippocampus of rats of acute carbon monoxide poisoning.5.Theδopioid receptor level of the frontal lobe was higher than hippocampus,and theδreceptor level rose generously from the 1st day to 28th day.Theκopioid receptor level of the frontal lobe was higher generously than hippocampus and striatum in the 3st day group and 14th day group.Theμopioid receptor level of striatum was generously higher than frontal lobe in 14th day group. Conclusion:1.This study found that there was a continuous change inδandκopioid receptor,however,μopioid receptor was overall not changed in frontal lobe,striatum and hippocampus of rats of acute carbon monoxide poisoning.2.δopioid receptor could be involved in defense response of hypoxia and ischemia and so on,which were caused by carbon monoxide poisoning.3.κopioid receptor could be involved in defense response of hypoxia and ischemia and so on,which were caused by carbon monoxide poisoning.Butκopioid receptor restrained the releasing of dopamine in striatum whenκopioid receptor was activated,which was related to the extrapyramidal syndrome after CO poisoning.
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