| The role of cyclooxygenase metabolities in the pathogeneticmechanism of endotoxin-induced acute lung injury in domestic pigs. |
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Chul Gyu Yoo, Ki Ho Jeong, Hyung Seok Choi, Hyuk Pyo Lee, Young Whan Kim, Sung Koo Han, Young Soo Shim, Keun Youl Kim, Yong Chol Han |
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Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea |
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| Abstract |
Background
lt has been suggested that the cycIooxygenase metabolites play an important role in changes of early hemodynamic parameters in the endotoxin.induced acute lung injury. But there have been many debates about their role in the late increase of alveolar-capillary permeability, and it is not known whether they act directly or indirectly through oxygen free radicals which have been known to be produced during the metabolic processs of cyclooxygenase pathway. So we performed this study to identify the pathogenetic role of cycIooxygenase metabolites in the endotoxin.induced acute lung injury in domestic pigs.
Methods
We infused endotoxin into 8 domestic pigs; endotoxin only (n=3), and pretreatment with indomethacin (n=5). We observed the sequential changes in hemodynamic parameters, the concentra.
tion of plasma oxidized glutathione (GSSG) in pulmonary arterial and venous blood, and albumin content in bronchoalveolar lavage fluid (BALF)
Results
1) While cardiac output decreased, mean pulmonary arterial pressure, pulmonary vascular resistance, and alveolar-arterial oxygen difference increased over phase 1 (Q- 2hr) and phase 2 (2-4 . 5hr) by endotoxin, indomethacin attenuated the decrease in cardiac output during phase 1 and increase in mean pulmonary arterial pressure, pulmonary vascular resistance, and alveolar-arterial oxygen difference during both phases.
2) The increase in plasma GSSG content during phase 2 was not attenuated by indomethacin.
3) The content of BALF albumin was significantly lower in indomethacin groups than that of endotoxin group.
Conclusion
These results suggest that it is likely that cycIooxygenase metabolites have an effect on endotoxin-induced acute lung injury during both phases probably through direct action. |
| Key Words:
Endotoxin, CycIooxygenase metabolites, Acute lung injury, Pigs |
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