| 颈动脉体损伤对COPD大鼠模型呼吸调控功能的影响 |
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| 引用本文： | 徐北政1,赵晓赟2,3,杨洋4,王菁5,刘珊6. 颈动脉体损伤对COPD大鼠模型呼吸调控功能的影响[J]. 天津医科大学学报, 2021, 0(4): 349-353 |
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| 作者姓名： | 徐北政1 赵晓赟2 3 杨洋4 王菁5 刘珊6 |
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| 作者单位： | （1.天津医科大学基础医学院,天津 300070;2.天津医科大学胸科临床学院,天津300222;3.天津市胸科医院呼吸与危重症医学科,天津 300222;4.天津市胸科医院内分泌科,天津 300222;5.天津市胸科医院病理科,天津 300222;6.天津市心血管疾病研究所,天津 300222） |
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| 摘 要： | 目的:探讨颈动脉体化学损伤对慢性阻塞性肺疾病（COPD）大鼠呼吸运动的影响。方法:根据随机数字表法,将30只Wistar大鼠分为两组,COPD组20只:用烟熏联合LPS气道内注药法建立大鼠COPD模型;对照组10只:同等条件饲养但不进行烟熏,气道内滴注生理盐水。实验组8周造模成功后,颈部正中切开暴露双侧颈动脉体（CB）,用双氧水浸润的滤纸条包裹颈总动脉分叉部,造成CB化学损伤;对照组在用同样方法分离暴露双侧颈总动脉后,用NS滤纸条包裹,对CB进行假损伤处理。分别记录每组大鼠呼吸频率、呼气间期、吸气间期、吸呼比等呼吸生理指标及血气分析结果,并进行统计学分析。造模结束后取所有大鼠双侧CB行病理学观察。结果:呼吸生理指标:CB损伤前COPD组呼吸频率明显高于对照组（t=3.186,P=0.004）,CB损伤后COPD组呼吸频率更低（t=-3.266,P=0.003）、吸气时间更长（t=3.989,P<0.001）、吸呼比更高（t=6.103,
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| 关 键 词： | 慢性阻塞性肺疾病 大鼠模型 CB 化学感受器 呼吸调控 |
Effects of carotid body injury on respiratory regulation in COPD rat model |
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| XU Bei-zheng,ZHAO Xiao-yun,' target=_blank rel=external>,YANG Yang,WANG Jing,LIU Shan. Effects of carotid body injury on respiratory regulation in COPD rat model[J]. Journal of Tianjin Medical University, 2021, 0(4): 349-353 |
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| Authors: | XU Bei-zheng ZHAO Xiao-yun ' target=_blank rel=external> YANG Yang WANG Jing LIU Shan |
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| Affiliation: | （1.School of Basic Medical Sciences,Tianjin Medical University,Tianjin 300070,China;2.Clinical College of Thoracic Medicine,Tianjin Medical University,Tianjin 300222,China;3.Department of Pulmonary and Critical Care Medicine,Tianjin Chest Hospital,Tianjin 300222,China;4.Department of Endocrinology,Tianjin Chest Hospital,Tianjin 300222,China;5.Department of Pathology,Tianjin Chest Hospital,Tianjin 300222,China;6.Tianjin Institute of Cardiovascular Disease,Tianjin 300222,China） |
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| Abstract: | Objective: To investigate the effect of carotid body chemical injury on respiratory movement in rats with chronic obstructive pulmonary disease（COPD）. Methods: According to the method of random number table,30 Wistar rats were divided into two groups: the COPD group（n=20） and the control group（n=10）. The COPD model was established by fumigation combined with LPS intratracheal injection,and the control group（n=10） was fed without fumigation under the same conditions and intratracheal instillation of normal saline. In the experimental group,after 8 weeks of successful modeling,the bilateral carotid body（CB） was exposed by median cervical incision,and the bifurcation of the common carotid artery was wrapped with a filter strip infiltrated with hydrogen peroxide,resulting in chemical injury of the common carotid body,while in the control group,after the bilateral common carotid artery was separated and exposed with the same method,the bilateral common carotid artery was wrapped with NS filter paper,and the carotid body was treated with sham injury. The respiratory physiological indexes such as respiratory frequency,expiratory interval,inspiratory interval,inspiratory/expiratory ratio and the results of blood gas analysis in each group were recorded and statistically analyzed. After the establishment of the model,the bilateral carotid arteries of all rats were taken for pathological observation. Results: Respiratory physiological indexes: the respiratory rate of COPD rats before CB injury was significantly higher than that of the control group（t=3.186,P=0.004）. After CB injury,the respiratory rate of COPD rats was lower（t=-3.266,P=0.003）,the inspiratory time was longer （t=3.989,P<0.001） and the inspiratory/expiratory ratio was higher than that of the control group（t=6.103,P<0.001）. Self-control showed that the respiratory rate decreased in both COPD rats and control rats after CB injury（control group t1=5.136,COPD group t2=9.656,P<0.001）. Results of blood gas analysis: plasma pH and arterial oxygen partial pressure of COPD rats before and after CB injury were lower than those of control group,while partial pressure of carbon dioxide were higher than those of control group（inter-group control before injury tpH=-5.996,t■=11.640,t■=-3.415,inter-group control after injury tpH=-13.874,t■=13.475,t■=-17.295;self-control of COPD group before and after injury tpH=-13.781,t■=4.341, |
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| Keywords: | chronicobstructive pulmonary disease rat model carotid body chemoreceptor respiratory regulation |
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