[Pulmonary fibrosis after endotoxin-induced permeability edema].
To know the pathogenesis of the lung fibrosis after ARDS, we investigated the role of PMN-elastase after endotoxin-induced pulmonary edema in awake sheep with chronic lung lymph fistulas. The permeability of the pulmonary circulation increased 2 hours after endotoxin injection. Four hours after endotoxin injection, WBC migrated to the lung interstitium and the number of WBC in BALF increased. Endotoxin increased PMN-elastase in plasma and lymph whereas the level of alpha-1-protease inhibitor (alpha-1-PI) did not change. The activity of alpha-1-PI measured by trypsin inhibitory capacity was zero in the exudative phase. The level of PMN-elastase in lymph was significantly higher 1 week after endotoxin injection than baseline levels. Histologically, pulmonary fibrosis developed 1 week after endotoxin injection. These results suggest that inflammatory mediators released from PMN play an important part in progress to the fibrotic phase after ARDS.
Koike
K
K
Chida
M
M
Suzuki
S
S
Ashino
Y
Y
Kubo
Y
Y
Isogami
K
K
Nasu
G
G
Ono
S
S
Sagara
Y
Y
Sakuma
T
T
D000818:Animals; D004731:Endotoxins; D008168:Lung / Q000473:pathology*; D009504:Neutrophils / Q000378:metabolism; D010196:Pancreatic Elastase / Q000378:metabolism*; D011654:Pulmonary Edema / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D011658:Pulmonary Fibrosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D012756:Sheep; D000515:alpha 1-Antitrypsin / Q000378:metabolism
D004731:Endotoxins; D000515:alpha 1-Antitrypsin; D010196:Pancreatic Elastase