Establishment of a rat model of COPD-OSAHS overlap syndrome induced by smoking and intermittent hypoxia
Received:August 06, 2018  
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DOI:10. 3969 / j.issn.1005-4847. 2019. 01. 010
KeyWord:emphysema; smoking; intermittent hypoxia; sleep apnea hypopnea; overlap syndrome; model; rat
                          
AuthorInstitution
陈敏 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
黄照明 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
何剑 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
毕虹 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
王清 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
何乐伟 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
杜俊毅 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
周开华 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
金志贤 昆明市第一人民医院甘美医院呼吸与危重症医学科,昆明 
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Abstract:
      Objective To establish a rat model of chronic obstructive lung disease (COPD) and obstructive sleep apnea-hypopnea synclrome(OSAHS) overlap syndrome (OS), which can provide a feasible means and experimental platform for basic research on the overlap syndrome. Methods 14 SPF female 6-week-old SD rats were randomly divided into experimental group (n = 8) and control group (n = 6). The rats in experimental group were exposed to smoke and intermittent hypoxia environment, and the rats in control group were given sham smoke and normal oxygen. After 8 weeks,the survival rate of rats in experimental group was calculated, and the general condition, blood gas analysis, right ventricular hypertrophy index, mean alveolar numbers, mean alveolar septum, and pathological changes of lung tissue were compared between the two groups. Results The oxygen concentration-time curve of intermittent hypoxic chamber showed that oxygen concentration decreased periodically and returned to normal, which indicated that the intermittent hypoxic gas environment was successfully simulated. At last, 6 rats in the experimental group survived, with a survival rate of 75%,while all rats in control group survived. Compared with the control group, the 6 surviving SD rats in experimental group were generally in poor condition, with acidosis, hypoxemia and carbon dioxide retention, right ventricular hypertrophy,significantly increased mean alveolar intercept and significantly decreased mean alveolar number ( P < 0. 05). The difference was statistically significant. Pathological observation of lung tissue showed that pulmonary interstitial inflammatory infiltration, lymphocyte proliferation in bronchial wall, smooth muscle hyperplasia in bronchial wall, partial rupture of smooth muscle in bronchial wall, goblet cells hyperplasia and emphysema. Conclusions A rat model of OS is successfully established by smoking and intermittent hypoxia exposure. More meaningful and objective evaluation indicators of the OS model are still to be found.
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