中国医科大学学报
中國醫科大學學報
중국의과대학학보
JOURNAL OF CHINA MEDICAL UNIVERSITY
2010年
6期
422-424
,共3页
甲型流感病毒%β1-肾上腺素能受体激动剂%肺泡液体清除率
甲型流感病毒%β1-腎上腺素能受體激動劑%肺泡液體清除率
갑형류감병독%β1-신상선소능수체격동제%폐포액체청제솔
influenza virus A%β1-adrenergic agonist%alveolar fluid clearance
目的探讨甲型流感病毒（A/PR/8/34株,H1N1）对在体大鼠肺泡液体清除率（AFC）的影响,以及β1-肾上腺素能受体激动剂地诺帕明对于在体大鼠AFC的影响机制。方法将SD大鼠分为正常对照组、H1N1感染模型组、感染后地诺帕明干预组。研究H1N1感染后AFC的变化以及地诺帕明的调节作用,并应用ELISA方法检测肺组织内环腺苷酸（cAMP）、环鸟苷酸（cGMP）的水平。结果正常对照组AFC为（17.25±1.01）%,肺干湿重比（W/D）为4.99±0.02;H1N1感染组AFC降为（9.15±1.01）%,W/D升高至6.77±0.13。干预组可以显著地提高H1N1感染后的AFC[（14.41±1.41）%],W/D为5.98±0.22。正常肺组织内cAMP活性为（2.73±0.06）nmol·mg-1·mg-1,cGMP的活性为（5.10±1.88）pmol·mg-1·mg-1。H1N1感染组肺组织内的cAMP明显下降[（1.43±0.06）nmol·mg-1·mg-1],cGMP水平升高[（7.34±0.40）pmol·mg-1·mg-1],应用地诺帕明可以提高肺组织内的cAMP的活性[（2.06±0.16）nmol·mg-·1mg-1],cGMP的活性下降为[（6.16±1.36）pmol·mg-·1mg-1]。结论 H1N1感染可导致大鼠AFC明显下降、肺水肿加重。地诺帕明可以提高在体H1N1感染大鼠模型的AFC、减轻肺水肿,并可以逆转感染组cAMP/cGMP的下降。说明β1-肾上腺素能受体激动剂提高AFC及减低肺水肿可能是通过cAMP-PKA信号转导途径完成。
目的探討甲型流感病毒（A/PR/8/34株,H1N1）對在體大鼠肺泡液體清除率（AFC）的影響,以及β1-腎上腺素能受體激動劑地諾帕明對于在體大鼠AFC的影響機製。方法將SD大鼠分為正常對照組、H1N1感染模型組、感染後地諾帕明榦預組。研究H1N1感染後AFC的變化以及地諾帕明的調節作用,併應用ELISA方法檢測肺組織內環腺苷痠（cAMP）、環鳥苷痠（cGMP）的水平。結果正常對照組AFC為（17.25±1.01）%,肺榦濕重比（W/D）為4.99±0.02;H1N1感染組AFC降為（9.15±1.01）%,W/D升高至6.77±0.13。榦預組可以顯著地提高H1N1感染後的AFC[（14.41±1.41）%],W/D為5.98±0.22。正常肺組織內cAMP活性為（2.73±0.06）nmol·mg-1·mg-1,cGMP的活性為（5.10±1.88）pmol·mg-1·mg-1。H1N1感染組肺組織內的cAMP明顯下降[（1.43±0.06）nmol·mg-1·mg-1],cGMP水平升高[（7.34±0.40）pmol·mg-1·mg-1],應用地諾帕明可以提高肺組織內的cAMP的活性[（2.06±0.16）nmol·mg-·1mg-1],cGMP的活性下降為[（6.16±1.36）pmol·mg-·1mg-1]。結論 H1N1感染可導緻大鼠AFC明顯下降、肺水腫加重。地諾帕明可以提高在體H1N1感染大鼠模型的AFC、減輕肺水腫,併可以逆轉感染組cAMP/cGMP的下降。說明β1-腎上腺素能受體激動劑提高AFC及減低肺水腫可能是通過cAMP-PKA信號轉導途徑完成。
목적탐토갑형류감병독（A/PR/8/34주,H1N1）대재체대서폐포액체청제솔（AFC）적영향,이급β1-신상선소능수체격동제지낙파명대우재체대서AFC적영향궤제。방법장SD대서분위정상대조조、H1N1감염모형조、감염후지낙파명간예조。연구H1N1감염후AFC적변화이급지낙파명적조절작용,병응용ELISA방법검측폐조직내배선감산（cAMP）、배조감산（cGMP）적수평。결과정상대조조AFC위（17.25±1.01）%,폐간습중비（W/D）위4.99±0.02;H1N1감염조AFC강위（9.15±1.01）%,W/D승고지6.77±0.13。간예조가이현저지제고H1N1감염후적AFC[（14.41±1.41）%],W/D위5.98±0.22。정상폐조직내cAMP활성위（2.73±0.06）nmol·mg-1·mg-1,cGMP적활성위（5.10±1.88）pmol·mg-1·mg-1。H1N1감염조폐조직내적cAMP명현하강[（1.43±0.06）nmol·mg-1·mg-1],cGMP수평승고[（7.34±0.40）pmol·mg-1·mg-1],응용지낙파명가이제고폐조직내적cAMP적활성[（2.06±0.16）nmol·mg-·1mg-1],cGMP적활성하강위[（6.16±1.36）pmol·mg-·1mg-1]。결론 H1N1감염가도치대서AFC명현하강、폐수종가중。지낙파명가이제고재체H1N1감염대서모형적AFC、감경폐수종,병가이역전감염조cAMP/cGMP적하강。설명β1-신상선소능수체격동제제고AFC급감저폐수종가능시통과cAMP-PKA신호전도도경완성。
Objective To investigate the influence of influenza virus A（H1N1,A/PR/8/34 strain）on alveolar fluid clearance（AFC）in vivo and the effects of β1-adrenergic agonist on AFC in rat lungs infected by H1N1.Methods Fortyfive rats were divided into control group（n =12）,H1N1 infection group（the rats were infected with influenza virus strain A/PR/8/34,n =18）,β1-adrenergic agonist groups（the rats were administrated with β1-adrenergic agonist after HIN1 infection,n =15）.AFC was estimated by the progressive increase in the albumin concentration over 30 minutes.The activity of cAMP and cGMP in the lung tissues of control,H1N1 infection and β1-adrenergic agonist groups was measured.Results The infection with H1N1 resulted in a decline in AFC 9.15±1.01% vs control group 17.25±1.01% and increased lung water content（W/D was 6.77±0.13 vs control group 4.99±0.02）.H1N1-mediated inhibition of AFC could be reversed to 14.41±1.41% by the administration of β1-adrenergic agonist denopamine.H1N1 infection increased cGMP levels 7.34±0.40 pmol·mg-1· mg-1 vs control group 5.10±1.88 pmol·mg-1·mg-1 and decreased cAMP levels 1.43±0.06 nmol·mg-1·mg-1 in lung tissues compared with control group.β1-agonist denopamine reversed the level of cAMP to 2.06±0.16 nmol·mg-1·mg-1 and cGMP to 6.16±1.36 pmol·mg-1·mg-1.Conclusion H1N1 infection decreased AFC and increased lung edema.β1-agonist denopamine could reverse AFC and the ratio of cAMP/cGMP in H1N1 infected lung tissues.β1-agonist might regulate AFC through the pathway of cAMP-PKA.
