2002Zhonghua mazuixue zazhiRequires access

The role of p38 mitogen-activated protein kinase in the injury induced by mechanical ventilation

Huixiang Chen

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Abstract

Objective The purpose of this study was to investigate the role of p38 mitogen-activated protein kinase ( p38 MAPK) in the lung injury induced by mechanical ventilation.Methods Fifteen healthy 80 day-old pigs weighing (22.5 ± 1.5)kg were randomly divided into three groups according to the tidal volume(VT) and PEEP of mechanical ventilation: group A (VT = 16ml·kg-1, PEEP = 0) ; group B (VT = 6 ml·kg-1, PEEP= 16cm H2O) and group C(VT = 16ml·kg-1, PEEP = 8cm H2O). The animals were mechanically ventilated for 3h, then sacrificed by exsanguination. Right lower lobe was immediately removed for identification of intercellular adhesion molecule-1 ( ICAM-1 ) expression using immunohistological technique, determination of phosphorylated p38 MAPK content using Western Blot and microscopic examination. Results There was significant histological changes in the lung tissue in group A and B, but no significant histological changes were found in group C. The expression of ICAM-1 was positive in the lung in group A and B but negative in group C. The level of phosphorylated p38 MAPK among the 3 groups. Conclusion Acute lung injury can be induced by mechanical ventilation with high tidal volume or low tidal volume plus high PEEP, p38 MAPK may mediate the inflammatory response-induced lung injury.

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Objective The purpose of this study was to investigate the role of p38 mitogen-activated protein kinase ( p38 MAPK) in the lung injury induced by mechanical ventilation.Methods Fifteen healthy 80 day-old pigs weighing (22.5 ± 1.5)kg were randomly divided into three groups according to the tidal volume(VT) and PEEP of mechanical ventilation: group A (VT = 16ml·kg-1, PEEP = 0) ; group B (VT = 6 ml·kg-1, PEEP= 16cm H2O) and group C(VT = 16ml·kg-1, PEEP = 8cm H2O). The animals were mechanically ventilated for 3h, then sacrificed by exsanguination. Right lower lobe was immediately removed for identification of intercellular adhesion molecule-1 ( ICAM-1 ) expression using immunohistological technique, determination of phosphorylated p38 MAPK content using Western Blot and microscopic examination. Results There was significant histological changes in the lung tissue in group A and B, but no significant histological changes were found in group C. The expression of ICAM-1 was positive in the lung in group A and B but negative in group C. The level of phosphorylated p38 MAPK among the 3 groups. Conclusion Acute lung injury can be induced by mechanical ventilation with high tidal volume or low tidal volume plus high PEEP, p38 MAPK may mediate the inflammatory response-induced lung injury.

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Available abstract

Objective The purpose of this study was to investigate the role of p38 mitogen-activated protein kinase ( p38 MAPK) in the lung injury induced by mechanical ventilation.Methods Fifteen healthy 80 day-old pigs weighing (22.5 ± 1.5)kg were randomly divided into three groups according to the tidal volume(VT) and PEEP of mechanical ventilation: group A (VT = 16ml·kg-1, PEEP = 0) ; group B (VT = 6 ml·kg-1, PEEP= 16cm H2O) and group C(VT = 16ml·kg-1, PEEP = 8cm H2O). The animals were mechanically ventilated for 3h, then sacrificed by exsanguination. Right lower lobe was immediately removed for identification of intercellular adhesion molecule-1 ( ICAM-1 ) expression using immunohistological technique, determination of phosphorylated p38 MAPK content using Western Blot and microscopic examination. Results There was significant histological changes in the lung tissue in group A and B, but no significant histological changes were found in group C. The expression of ICAM-1 was positive in the lung in group A and B but negative in group C. The level of phosphorylated p38 MAPK among the 3 groups. Conclusion Acute lung injury can be induced by mechanical ventilation with high tidal volume or low tidal volume plus high PEEP, p38 MAPK may mediate the inflammatory response-induced lung injury.

Key concepts: Mechanical ventilation, p38 mitogen-activated protein kinases, Tidal volume, Ventilation (architecture), Lung, Western blot, MAPK/ERK pathway, Kinase

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