A model of delayed encephalopathy acute carbon monoxide poisoning established with inhalation method
CHEN Chao1 WANG Baojun2 XIANG Wenping2 LI Yuechun2 HAO Xiwa2 PANG Jiangxia2 GAO Haoran2 XIE Wei3
1.Department of Neurology, Center Hospital of Baotou, Inner Mongolia Medical University, Inner Mongolia Autonomous Region, Baotou 014000, China;
2.Department of Neurology, Center Hospital of Baotou, Inner Mongolia Autonomous Region, Baotou 014000, China;
3.Central Laboratory, Baotou Medical College, Inner Mongolia Autonomous Region, Baotou 014000, China
Abstract：Objective To establish a model of delayed encephalopathy acute carbon monoxide poisoning (DEACMP). Methods A total of 196 intelligence-qualified rats were divided into experimental group and control group by random number table method, with 164 rats in the experimental group and 32 rats in the control group. The experimental group used an acute static inhalation of carbon monoxide (CO) to establish a poisoned rat model. According to different concentrations of CO poisoning, they were randomly divided into 1000, 3000, 4000 ppm group, with 32 rats alive in each group. Each group continued to inhale for 40 minutes. Rats in each group were sacrificed at 7, 14, 21 and 28 d after poisoning. Spectrophotometer method was used to dynamically monitor the changes of carboxyhemoglobin (COHb) content in each group. Morris water maze test was used to evaluate cognitive function. HE staining was used to observe the cell damage in hippocampus. The best poisoning concentration and time for establishing a DEACMP rat model was established. Results After poisoned by CO, the rats showed typical symptoms of poisoning. There was a significant positive correlation between COHb content and CO concentration (r = 0.748, P ＜ 0.05). The mortality rates of the 1000, 3000, 4000 ppm group and the control group were 0%, 40.74%, 58.97% and 0%, respectively. The incidence of DEACMP in each group was 0%, 6.25%, 28.13%, 31.25%, and 0%, and the 21 d and 28 d after being poisoned were high DEACMP time points. Based on the low mortality rate and high incidence rate, the CO poisoning concentration of 3000 ppm and the time of 21d were the best method to establish a DEACMP rat model. Conclusion A DEACMP rat model can be established with a static inhalation concentration of 3000 ppm CO for 40 minutes, and models can be successfully established 21 days after poisoning.
[1] Rose JJ，Wang L，Xu Q，et al. Carbon monoxide poisoning：pathogenesis，management，and future directions of therapy [J]. Am J Respir Crit Care Med，2017，195（5）：596-606.
[2] Borger J. The danger of carbon monoxide poisoning associated with hookah use：an emergency physician′s perspective [J]. N C Med J，2017，78（6）：424.
[3] McKenzie LB，Roberts KJ，Shields WC，et al. Distribution and Evaluation of a Carbon Monoxide Detector Intervention in Two Settings：Emergency Department and Urban Community [J]. J Environ Health，2017，79（9）：24-30.
[4] Wang B，Xiang W，Xue H，et al. Efficacy of N-Butylphthalide and hyperbaric oxygen therapy on cognitive dysfunction in patients with delayed encephalopathy after acute carbon monoxide poisoning [J]. Med Sci Monit，2017， 23：1501-1506.
[5] Jorge A. Carbon monoxide poisoning [J]. Crit Care Clin，2012， 28：537-548.
[6] Goldstein M. Carbon monoxide poisoning [J]. J Emerg Nurs，2008，34：538-542.
[7] Xiang W，Xue H，Wang B，et al. Combined application of dexame-thasone and hyperbaric oxygen therapy yields better efficacy for patients with delayed encephalopathy after acute carbon monoxide poisoning [J]. Drug Des Devel Ther，2017，11：513-519.
[8] Hara S，Mizukami H，Kurosaki K，et al. Existence of a threshold for hydroxyl radical generation independent of hypoxia in rat striatum during carbon monoxide poisoning [J]. Arch Toxicol，2011，85：1091-1099.
[9] Hara S，Mizukami H，Kuriiwa F，et al. cAMP production mediated through P2Y（11）-like receptors in rat striatum due to severe，but not moderate，carbon monoxide poisoning [J]. Toxicology，2011，288：49-55.
[10] Ochi S，Abe M，Li C，et al. The nicotinic cholinergic system is affected in rats with delayed carbon monoxide encephalopathy [J]. Neurosci Lett，2014，569：33-37.
[11] Sun X，Xu H，Meng X，et al. Potential use of hyperoxygenated solution as a treatment strategy for carbon monoxide poisoning [J]. PLoS One，2013，8（12）：e81779.
[12] Guan L，Zhang YL，Li ZY，et al. Salvianolic acids attenuate rat hippocampal injury after acute CO poisoning by improving blood flow properties [J]. Biomed Res Int，2015，2015：526483.
[13] Xiang WP，Xue H，Wang BJ，et al. Delayed encephalopathy of acute carbon monoxide intoxication in rats：potential mechanism and intervention of dexamethasone [J]. Pak J Pharm Sci，2014，27：2025-2028.
[14] Chen Q，Bai J，Li CR，et al. Changes of HbCO in the blood of rats with different CO concentration and inhalation time [J]. Fa Yi Xue Za Zhi，2016，32（6）：410-412.
[15] Li Q，Bi MJ，Bi WK，et al. Edaravone attenuates brain damage in rats after acute CO poisoning through inhibiting apoptosis and oxidative stress [J]. Environ Toxicol，2016，31（3）：372-379.
[16] Roderique JD，Josef CS，Newcomb AH，et al. Preclinical evaluation of injectable reduced hydroxocobalamin as an antidote to acute carbon monoxide poisoning [J]. J Trauma Acute Care Surg，2015，79：116-120.
[17] Zhang J，Wu H，Zhao Y，et al. Therapeutic effects of hydrogen sulfide in treating delayed encephalopathy after acute carbon monoxide poisoning [J]. Am J Ther，2016， 23（6）：e1709-e1714.
[18] Li HM，Shi YL，Wen D，et al. A novel effective chemical hemin for the treatment of acute carbon monoxide poisoning in mice [J]. Exp Ther Med，2017，14（5）：5186-5192.
[19] Xue L，Wang WL，Li Y，et al. Effects of hyperbaric oxygen on hippocampal neuronal apoptosis in rats with acute carbon monoxide poisoning [J]. Undersea Hyperb Med，2017，44（2）：121-131.
[20] Watanabe S，Matsuo H，Kobayashi Y，et al. Transient degradation of myelin basic protein in the rat hippocampus following acute carbon monoxide poisoning [J]. Neurosci Res，2010，68（3）：232-240.
2019, Vol. 16 
京公网安备 11010502046598号