Correlation between memory deficit and delayed neuronal damage after carbon monoxide poisoning in rats
- VernacularTitle:急性一氧化碳中毒大鼠记忆功能改变与迟发性神经元损伤的相关性
- Author:
Yizhan CAO
;
Xing JIN
;
Qing ZHA
;
Boliang WANG
;
Yuexia ZHONG
;
Guoqiang FU
;
Baojian HE
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2007;11(29):5832-5835
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Acute carbon monoxide (CO) poisoning may lead to delayed amnesia in rats,and which is similar to delayed neurologic syndrome caused by acute CO in human.So,this experiment is to investigate the pathogenesis of delayed neurologic syndrome by studying acute CO poisoning in the rats.OBJECTIVE:To observe the changes in delayed neuronal damage and memory after acute CO poisoning in the rats,and analyze their correlation.DESIGN:Randomized controlled animal experiment.SETTING:Department of Emergency,Tangdu Hospital,Fourth Military Medical University of Chinese PLA;Department of Laboratory Medicine,Xi'an Gaoxin Hospital;The General Hospital of the Air Force of Chinese PLA,Center for Hyperbaric Oxygen Treatment,Department of Aerospace Medicine,Fourth Military Medical University of Chinese PLA.MATERIALS:This experiment was carried out in the Laboratory of Aviation Pathology and Molecular Biology,Department of Aerospace Medicine.Fourth Military Medical University of Chinese PLA from July to November 2005.Fiftyhealthy male Sprague-Dawley(SD)rats were randomized into control group and CO poisoning group,with 25 rats each.METHODS:The awake rats in the CO poisoning group were placed in self-made jar for poisoning,then which was pumped with 0.999 volume fraction of CO.Rats in the jar inhaled the mixture of CO and air for 60 minutes.The average volume fraction of CO in the jar was 3.451×10-3.Rats in the control group were untouched.MAIN OUTCOME MEASURES:①The step down test was carried out in the rats before and 1,3,5 and 7 days after Coexposure.Escape latency was used as an index for evaluating the ability of memory retention.Shorter escape latencyindicated poor memory ability.②Pathological changes of brain tissue:After step down test was carried out following 1,3,5 and 7 days of CO exposure,6 rats were separately sacrificed in each group,and their brains were harvested.The brain tissue sections were performed haematoxylin & eosin (HE) staining for observing pathological injury degree and the amount of pyramidal neurons in hippocampal CA1 region.③SPSS 10.0 software was used to analyze the relationship of the amount of pyramidal neurons in hippocampal CA1 region and escape latency.RESULTS:Forty-eight rats were involved in the final analysis.①There were no significant differences in escape latencyon the 1"and 3"days after CO exposure between two groups. but escape latency in the CO poisoning group was significantly shorter than that in the control group on the 5th and 7th days after CO exposure(P＜0.05,0.01).②There were no significant changes in the amount of pyramidal neurons in hippocampal CA1 region on the 1st day after CO exposure between CO poisoning group and control group,but pyramidal neurons in hippocampal CA1 region in the CO poisoning group were significantly reduced on the 3rd,5th and 7th days after CO exposure,and 1 5%dead pyramidal neurons were found on the 7th day after CO exposure.③Decrease of pyramidal neurons in hippocampal CA1 region was significantly correlated with shortening of escape latency of rats in the CO poisoning group(r=0.270,P＜0.01).CONCLUSION:Acute CO poisoning leads to delayed neuronal damage,which causes delayed amnesia.
