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The Influence of Influenza Virus A on Alveolar Fluid Clearance in Rat Lungs / 中国医科大学学报
Journal of China Medical University ; (12): 422-424, 2010.
Artigo em Chinês | WPRIM | ID: wpr-432609
ABSTRACT
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.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of China Medical University Ano de publicação: 2010 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of China Medical University Ano de publicação: 2010 Tipo de documento: Artigo