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The role of complement and neutrophils in air bubble-induced lung injury
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|Title:||The role of complement and neutrophils in air bubble-induced lung injury|
|Abstract:||Pulmonary air embolism causes vascular obstruction and induces biochemical reactions leading to lung injury. In the present study, by using isolated and perfused rat lungs, we investigated the involvement of the complement system and polymorphonuclear leukocytes (P:MN) in the alterations of segmental vascular resistances, lung weight gain, and filtration coefficient (K), a measure of vascular permeability. After establishing ventilation with air and 5% CO2, the lung was removed en bloc and suspended in a humidified chamber at 37°C. Lung weight, arterial and venous pressures were monitored continuously. Lungs were perfused with physiological salt solution (PSS) containing 4% Ficoll. We used 6 series of perfusates containing: 1) PSS, 2) PMN, 3) plasma, 4) decomplemented plasma, 5) PMN and plasma, and 6) PMN and decomplemented plasma. Air embolism, induced by a 0.76-ml air infusion to arterial catheter in 20 min, increased arterial pressure without altering capillary and venous pressure, suggesting that the increased arterial resistance alone was responsible for the pulmonary hypertension. In lungs perfused with both PMN and normal plasma, air embolism increased Kf by 145 ± 190% which was significantly greater than those in lungs perfused with either PMN (91 ± 8%), plasma (90 ± 8%), or PMN and decomplemented plasma (80 ± 9%). Air embolism increased Kf by 45 ± 12% in the lungs perfused with decomplemented plasma, which was the least among groups. These results suggest that air embolism damages the lung by hypertension, activation of the complement, and activation of PMN, singly or in combinations. The modulation role of PMN in air bubble-induced lung injury was investigated by pretreating the lungs with blocking agents of the cytotoxic substances released from PMN. The lungs perfused with both P:MN and normal plasma served as the control group. In lungs pretreated with scavengers, air embolism increased Kr by 108 ± 25% which was not different from the control group. Air embolism induced little change of Kf in the lungs pretreated with indomethacin (17 ± 8%) or isoproterenol (0 ± 9%), suggesting that air embolism increases pulmonary vascular permeability involving the release of arachidonic acid metabolites.|
|Description:||Thesis (Ph. D.)--University of Hawaii at Manoa, 1995.|
Includes bibliographical references (leaves 149-171).
xvi, 171 leaves, bound ill. 29 cm
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|Appears in Collections:||Ph.D. - Biomedical Sciences (Physiology)|
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