2004Unpublished venueRequires access

The changes and its significances of interleukin-6 and interferon-α of lung tissue in rats after smoke inhalation injury

Yang Tian-de

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Abstract

Objective To explore the changes and its significance of interleukin-6(IL-6) and interferon-α(INFα)of lung tissue in rats after smoke inhalation injury.Methods The model of smoke inhalation injury in rat was set up,sixty Wistar rats were randomly divided into six groups such as control group ,and the groups of 1h,3h,6h,12h and 24h following smoke inhalation.The lung tissue was isolated and the blood samples were get,and the data of blood gases and the water content of lung tissue were measured.The pulmonary vasopermeability was detected with 131 I-albumin exudation, TNF-α, IL-6 and INFαin lung tissue homogenate were assayed by radio-immunization and enzyme-linked immunosorbentassay(ELISA) respectively.Results Arterial PaO 2 from 1h to 24h following smoke inhalation were significantly lower than it in control group,but PaCO 2 in groups of 12h and 24h after smoke inhalation were markedly higher than it in control group.The water content and 131 I-albumin exudation of lung tissue from 1h to 24h following smoke inhalation were obviously increased while comparing with control group.TNF-αcontent in lung homogenate from 1h to 24h following smoke inhalation and IL-6 content in lung homogenate from 1h to 12h following smoke inhalation were remarkably higher than it in control group,and INF-α content in lung tissue homogenate only in 6h group after smoke inhalation was obviously higher than it in control group.Conclusion The increases in of IL-6 and INF-αin lung tissue after smoke inhalation should imply that IL-6 and INF-α take part in the generating and developing of smoke inhalation injury,and the action of IL-6 be more early and more persistent.

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Objective To explore the changes and its significance of interleukin-6(IL-6) and interferon-α(INFα)of lung tissue in rats after smoke inhalation injury.Methods The model of smoke inhalation injury in rat was set up,sixty Wistar rats were randomly divided into six groups such as control group ,and the groups of 1h,3h,6h,12h and 24h following smoke inhalation.The lung tissue was isolated and the blood samples were get,and the data of blood gases and the water content of lung tissue were measured.The pulmonary vasopermeability was detected with 131 I-albumin exudation, TNF-α, IL-6 and INFαin lung tissue homogenate were assayed by radio-immunization and enzyme-linked immunosorbentassay(ELISA) respectively.Results Arterial PaO 2 from 1h to 24h following smoke inhalation were significantly lower than it in control group,but PaCO 2 in groups of 12h and 24h after smoke inhalation were markedly higher than it in control group.The water content and 131 I-albumin exudation of lung tissue from 1h to 24h following smoke inhalation were obviously increased while comparing with control group.TNF-αcontent in lung homogenate from 1h to 24h following smoke inhalation and IL-6 content in lung homogenate from 1h to 12h following smoke inhalation were remarkably higher than it in control group,and INF-α content in lung tissue homogenate only in 6h group after smoke inhalation was obviously higher than it in control group.Conclusion The increases in of IL-6 and INF-αin lung tissue after smoke inhalation should imply that IL-6 and INF-α take part in the generating and developing of smoke inhalation injury,and the action of IL-6 be more early and more persistent.

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Available abstract

Objective To explore the changes and its significance of interleukin-6(IL-6) and interferon-α(INFα)of lung tissue in rats after smoke inhalation injury.Methods The model of smoke inhalation injury in rat was set up,sixty Wistar rats were randomly divided into six groups such as control group ,and the groups of 1h,3h,6h,12h and 24h following smoke inhalation.The lung tissue was isolated and the blood samples were get,and the data of blood gases and the water content of lung tissue were measured.The pulmonary vasopermeability was detected with 131 I-albumin exudation, TNF-α, IL-6 and INFαin lung tissue homogenate were assayed by radio-immunization and enzyme-linked immunosorbentassay(ELISA) respectively.Results Arterial PaO 2 from 1h to 24h following smoke inhalation were significantly lower than it in control group,but PaCO 2 in groups of 12h and 24h after smoke inhalation were markedly higher than it in control group.The water content and 131 I-albumin exudation of lung tissue from 1h to 24h following smoke inhalation were obviously increased while comparing with control group.TNF-αcontent in lung homogenate from 1h to 24h following smoke inhalation and IL-6 content in lung homogenate from 1h to 12h following smoke inhalation were remarkably higher than it in control group,and INF-α content in lung tissue homogenate only in 6h group after smoke inhalation was obviously higher than it in control group.Conclusion The increases in of IL-6 and INF-αin lung tissue after smoke inhalation should imply that IL-6 and INF-α take part in the generating and developing of smoke inhalation injury,and the action of IL-6 be more early and more persistent.

Key concepts: Smoke inhalation, Inhalation, Smoke Inhalation Injury, Lung, Smoke, Medicine, Arterial blood, Anesthesia

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