The role of cyclooxygenase metabolities in the pathogeneticmechanism of endotoxin-induced acute lung injury in domestic pigs
| Autor: | Ki Ho Jeong, Sung Koo Han, Keun Youl Kim, Young Soo Shim, Chul Gyu Yoo, Hyuk Pyo Lee, Hyung Seok Choi, Yong Chol Han, Young Whan Kim |
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| Rok vydání: | 1992 |
| Předmět: |
Pulmonary and Respiratory Medicine
Cardiac output medicine.diagnostic_test biology business.industry Hemodynamics Venous blood Lung injury Pharmacology Cyclooxygenase pathway Infectious Diseases Bronchoalveolar lavage medicine.anatomical_structure Anesthesia medicine Vascular resistance biology.protein Cyclooxygenase business |
| Zdroj: | Tuberculosis and Respiratory Diseases. 39:42-54 |
| ISSN: | 2005-6184 1738-3536 |
| DOI: | 10.4046/trd.1992.39.1.42 |
| Popis: | Background:It has been suggested that the cyclooxygenase 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 process of cyclooxygenase pathway. So we performed this study to identify the pathogenetic role of cyclooxygenase metabolites in the endotoxin-induced acute lung injury in domestic pigs. Method: 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 concentration 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 (0-2hr) 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 cyclooxygenase metabolites have an effect on endotoxin-induced acute lung injury during both phases probably through direct action. |
| Databáze: | OpenAIRE |
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