The Science Journal of the American Association for Respiratory Care

1997 OPEN FORUM Abstracts

NEUTROPHIL ACTIVATION AND ADHESION MOLECULES IN VENTILATOR-INDUCED LUNG INJURY.

Hideaki Imanaka, MD, Motomu Shimaoka, MD, Noriyuki Ohta, MD, Masaji Nishimura, MD, Nobuyuki Taenaka, MD, Hiroshi Kiyono, MD, Nariaki Matsuura, MD. Surgical ICU, National Cardiovascular Center and ICU, Osaka University, Osaka, Japan.

Mechanical ventilation with high pressure/volume causes lung injury. Recent studies have demonstrated that a neutrophil-mediated inflammatory reaction is involved in the progression of ventilator-induced lung injury. We have hypothesized that adhesion molecule is increased in alveolar cells in such lung injury. Methods: Wistar rats were anesthetized with pentobarbital and tracheotomized. After muscular paralysis, they were ventilated for 40 min with pressure control mode, high (45 cm H_{2}O) or low (7 cm H_{2}O) peak inspiratory pressure (PIP). Zero PEEP and F_{1}O_{2} of 0.21 were used in both PIPs. At 40 min of ventilation, arterial blood gas and static compliance were analyzed. After the animals were sacrificed, total lung lavage was performed. The number of neutrophil/ macrophage in lavage fluid and the expression of adhesion molecules (Mac-1, ICAM-1) on the cells were analyzed to access the degree of inflammation in the lungs. Results: In a high PIP group, PaO_{2} decreased at 40 min (128 ± 24 mmHg at 5 min, and 45 ± 8 mmHg at 40 min), while in a low PIP group, a change in PaO_{2} was not significant (100 ± 30 mmHg, 84 ± 15 mmHg). In a high PIP group, lower inflection points appeared in compliance curves (20.2 ± 2.9 cm H_{2}O). The high PIP group showed a significant increase in infiltrated neutrophils into alveolar spaces and upregulation of ICAM-1 expression on neutrophils.

(See original for figures)

Conclusions: Inflammatory reaction including upregulation of adhesion molecules may be involved in the formation of ventilator-induced lung injury.

OF-97-091

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