Correlation between Memory Deficit and Delayed Neuronal Damage after Carbon Monoxide Poisoning in Rats

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. Fifty healthy 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 CO exposure. Escape latency was used as an index for evaluating the ability of memory retention. Shorter escape latency indicated 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 latency on the 1(superscript st) and 3(superscript rd) 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 5(superscript th) and 7(superscript th) 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 1(superscript sd) 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 3(superscript th), 5(superscript th)and 7(superscript th) days after CO exposure, and 15% dead pyramidal neurons were found on the 7(superscript th) day after CO exposure. ③ Decrease of pyramidal neurons in hippocampal CAl 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.