| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Research Abstract |
The aim of the study was to evaluate the lung tissue that was subjected to positive pressure ventilation, and to ascertain whether different areas of lung are subject to ventilator-induced lung injury (VILI) depends on body position. In addition, it was also investigated if inflammatory mediators played any roles for the development of VILI.
Experiment1 : The animals (12 white rabbits) were anesthetized and tracheostomized, and all were mechanically ventilated in IMV mode with an infant ventilator (V. I. P. Bird) at a rate of 30/min, peak inspiratory pressure (PIP) 30 cmHィイD22ィエD2O, TィイD2IィエD2 0.6 s, and inspiratory flow 10 L/min. The animals were randomly assigned to 2 groups according to body position (supine or prone). After the start of mechanical ventilation CT scanning was performed every 30 min. All animals were ventilated until pulmonary parenchymal opacification was detected by CT.
Measurements and results : CT radiographs revealed parenchymal opacification mainly in the lower a
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nd base regions. The time from the beginning of mechanical ventilation to the appearance of parenchymal opacification in the lungs ranged from 60 to 120 min in the supine group, and 60 to 270 min in the prone group. In the study, the regional location of VILI did not vary according to body position. Position did not affect the particular region damaged by VILI. Other anatomical factors may be more important in the development of VILI.
Experiment2 : Male Wistar rats were tracheotomized and ventilated by high pressure (45 cm HィイD22ィエD2O of peak inspiratory pressure, n=23) or, as a control, low pressure (7 cm HィイD22ィエD2O, n=13) with zero PEEP and inspired oxygen fraction of 0.21. After 40 min of comparative ventilation, lung lavage was performed in 20 rats from experimental group and 10 from the control for immunofluorescence analysis using anti-CD11b and anti-CD54 monclonal antibodies
Measurements and results : The high-pressure group had significantly greater neutrophil infiltration into alveolar spaces, upregulation of CD54 and CD11b on alveolar macrophages, and more TGF-β1 mRNA in lung tissues. Histological findings demonstrated more infiltrating neutrophils, destructive change of alveolar wall, and deposition of matrix in the high-pressure group. These results suggest that a series of proinflammatory reactions including the activation of neutrophils and macrophages and profibrogenetic process (e. g., TGF-β1 mRNA expression) and deposition of matrix may be involved in the course of ventilator-induced lung injury. Less
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