Am. J. Respir. Crit. Care Med., Vol 152, No. 1, 07 1995, 348-354.
Endotoxin-induced hydrogen peroxide production in intact pulmonary circulation of rat
Y Minamiya, S Abo, M Kitamura, K Izumi, Y Kimura, K Tozawa and S Saito
Second Department of Surgery, Akita University, School of Medicine, Japan.
Although the importance of free oxygen radical has been reported in acute
lung injury, the direct evidence in vivo model was lacking. We report a new
method, which for the first time allows direct detection of hydrogen
peroxide in the intact rat pulmonary microcirculation. We used the computer
image-analyzing system and 2',7'-dichlorofluorescin diacetate for the
marker of hydrogen peroxide production in vivo. A rat sepsis model was
produced by continuous infusion of endotoxin for 30, 60, and 120 min.
Hydrogen peroxide production in the pulmonary microcirculation of the
sepsis rat was higher than in the control rat at each time point (p <
0.01) and increased time-dependently (p < 0.01). Catalase (5,000 U/kg)
almost completely inhibited the hydrogen peroxide production in the sepsis
rat (p < 0.01). In high-power view, hydrogen peroxide was detected in
granulocytes that adhered to the capillaries and endothelial cells that
were adjoining adherent granulocytes. These observations suggest that
hydrogen peroxide in the endothelium was diffused from granulocytes. In
this study, we demonstrated direct evidence of hydrogen peroxide production
from adherent granulocytes in intact rat lung treated with endotoxin. We
conclude that endotoxin causes the granulocyte adhesion and oxidative
stress to the endothelium due to adherent granulocytes within 30 min in the
pulmonary microcirculation.
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Copyright © 1995 American Thoracic Society
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