国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2015年
5期
342-346
,共5页
慢性阻塞性肺疾病%呼吸功能%认知功能%脑代谢
慢性阻塞性肺疾病%呼吸功能%認知功能%腦代謝
만성조새성폐질병%호흡공능%인지공능%뇌대사
Chronic obstructive pulmonary disease%Respiratory function%Cognitive function%Cerebral metabolites
目的 探讨COPD模型大鼠呼吸功能、认知功能和海马区脑代谢物质子核磁共振波谱(1 HNMR)特征变化的相关性,初步解释COPD引起认知功能损害的致病机制.方法 建立COPD大鼠模型,同时设置对照组(n =12).HE染色观察各组大鼠肺组织以及海马组织的病理学变化;测定FEV0.3、FVC、吸气阻力(RI)、动态顺应性(Cdyn)和FEV0.3/FVC.血气分析仪测定大鼠血液中PaO2、PaCO2.Morris水迷宫实验测试大鼠学习记忆能力变化,利用1HNMR分析大鼠海马区N-乙酰天门冬氨酸(NAA)、胆碱复合物(Cho)、肌酸(Cr)、肌醇(MI)和谷氨酸(Glu)水平.结果 与对照组比较,COPD模型组大鼠肺泡扩张,间隔变窄、断裂,形成肺大疱,海马区组织椎体细胞脱落,排列疏松;同时COPD大鼠呼吸功能显著降低,认知功能显著减退;脑代谢物浓度均降低,其中NAA/Cr、Cho/Cr和Glu/Cr浓度降低差异具有统计学意义(t值为0.557~2.387,P<0.05);COPD大鼠肺功能指标(FEV0.3 /FVC和Cdyn)以及脑代谢物(NAA/Cr、Cho/Cr和Glu/Cr)与定位航行实验逃避潜伏期和空间探索实验逃避潜伏期均呈显著负相关,同时FEV0.3/FVC和Cdyn与NAA/Cr、Cho/Cr呈正相关.结论 COPD大鼠呼吸功能衰退可改变海马区脑代谢物水平,从而可能引起认知功能降低.
目的 探討COPD模型大鼠呼吸功能、認知功能和海馬區腦代謝物質子覈磁共振波譜(1 HNMR)特徵變化的相關性,初步解釋COPD引起認知功能損害的緻病機製.方法 建立COPD大鼠模型,同時設置對照組(n =12).HE染色觀察各組大鼠肺組織以及海馬組織的病理學變化;測定FEV0.3、FVC、吸氣阻力(RI)、動態順應性(Cdyn)和FEV0.3/FVC.血氣分析儀測定大鼠血液中PaO2、PaCO2.Morris水迷宮實驗測試大鼠學習記憶能力變化,利用1HNMR分析大鼠海馬區N-乙酰天門鼕氨痠(NAA)、膽堿複閤物(Cho)、肌痠(Cr)、肌醇(MI)和穀氨痠(Glu)水平.結果 與對照組比較,COPD模型組大鼠肺泡擴張,間隔變窄、斷裂,形成肺大皰,海馬區組織椎體細胞脫落,排列疏鬆;同時COPD大鼠呼吸功能顯著降低,認知功能顯著減退;腦代謝物濃度均降低,其中NAA/Cr、Cho/Cr和Glu/Cr濃度降低差異具有統計學意義(t值為0.557~2.387,P<0.05);COPD大鼠肺功能指標(FEV0.3 /FVC和Cdyn)以及腦代謝物(NAA/Cr、Cho/Cr和Glu/Cr)與定位航行實驗逃避潛伏期和空間探索實驗逃避潛伏期均呈顯著負相關,同時FEV0.3/FVC和Cdyn與NAA/Cr、Cho/Cr呈正相關.結論 COPD大鼠呼吸功能衰退可改變海馬區腦代謝物水平,從而可能引起認知功能降低.
목적 탐토COPD모형대서호흡공능、인지공능화해마구뇌대사물질자핵자공진파보(1 HNMR)특정변화적상관성,초보해석COPD인기인지공능손해적치병궤제.방법 건립COPD대서모형,동시설치대조조(n =12).HE염색관찰각조대서폐조직이급해마조직적병이학변화;측정FEV0.3、FVC、흡기조력(RI)、동태순응성(Cdyn)화FEV0.3/FVC.혈기분석의측정대서혈액중PaO2、PaCO2.Morris수미궁실험측시대서학습기억능력변화,이용1HNMR분석대서해마구N-을선천문동안산(NAA)、담감복합물(Cho)、기산(Cr)、기순(MI)화곡안산(Glu)수평.결과 여대조조비교,COPD모형조대서폐포확장,간격변착、단렬,형성폐대포,해마구조직추체세포탈락,배렬소송;동시COPD대서호흡공능현저강저,인지공능현저감퇴;뇌대사물농도균강저,기중NAA/Cr、Cho/Cr화Glu/Cr농도강저차이구유통계학의의(t치위0.557~2.387,P<0.05);COPD대서폐공능지표(FEV0.3 /FVC화Cdyn)이급뇌대사물(NAA/Cr、Cho/Cr화Glu/Cr)여정위항행실험도피잠복기화공간탐색실험도피잠복기균정현저부상관,동시FEV0.3/FVC화Cdyn여NAA/Cr、Cho/Cr정정상관.결론 COPD대서호흡공능쇠퇴가개변해마구뇌대사물수평,종이가능인기인지공능강저.
Objective To study the correlation among respiratory function,cognitive function,and hippocampal metabolites on changes of concentration detected by proton nuclear magnetic resonance spectroscopy (1 HNMR) in rats model with chronic obstructive pulmonary disease (COPD),and propose a preliminary explanation to the pathogenesis of cognitive impair caused by COPD.Methods COPD rats model was established,and control group was set up (n =12).Pathologic changes in hippocampus and lung of rats was observed through HE stain.0.3 s forced expiratory volume (FEV0.3),forced vital capacity (FVC),resistance index (RI),dynamic compliance (Cdyn),and FEV0.3/FVC were measured.Blood oxygen partial pressure (PaO2) and partial pressure of carbon dioxide (PaCO2) were determined in the blood of rats using blood gas analyzer.Morris water maze was used to evaluate the ability of learning and memory of rats.Levels of n-acetyl aspartate (NAA),choline compounds (Cho),creatine (Cr),myoinositol (MI) and glutamate (Glu) in rat hippocampus were analyzed by1 HNMR.Results In comparison with control group,alveolar expansion,narrow interval,fracture,and formation of pulmonary bulla were observed in lung,and the drop of vertebral body cell and loose arrangement in hippocampus tissue.Simultaneously,respiratory function and cognitive function were significantly lower in the group of COPD rats model.Concentration of cerebral metabolites,such as NAA/Cr,Cho/Cr and Glu/Cr,significantly decreased as compared to control group (with t values from 0.557 to 2.387,P <0.05).In COPD model,significant negative correlation was observed between lung function indexs (FEV0.3/FVC and Cdyn) as well as cerebral metabolites (NAA/Cr,Cho/Cr and Glu/Cr) and not only navigation experiment escape latency but also space exploration escape latency,and at the same time lung these function indexs displayed a positive correlation with NAA/Cr and Cho/Cr.Conclusions The recession of respiratory function caused by COPD could change levels of cerebral metabolites in the hippocampus,and may impair cognitive function thereby.