NPC 15669 blocks neutrophil CD18 increase and lung injury during cardiopulmonary bypass in pigs
Autor: | K. J. Zehr, Jenny M. Bator, R. M. Burch, J. R. Connor, A M Gillinov, Duke E. Cameron, Ian C. Wilson, J. M. Redmond, Ahvie Herskowitz |
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Rok vydání: | 1992 |
Předmět: |
Pathology
medicine.medical_specialty Immunology CD18 Lung injury law.invention law lcsh:Pathology medicine Cardiopulmonary bypass Lung biology business.industry Cell Biology medicine.disease Extravasation Cellular infiltration medicine.anatomical_structure surgical procedures operative Myeloperoxidase biology.protein business Infiltration (medical) lcsh:RB1-214 circulatory and respiratory physiology Research Article |
Zdroj: | Mediators of Inflammation Mediators of Inflammation, Vol 2, Iss 2, Pp 135-141 (1993) |
ISSN: | 0962-9351 |
Popis: | During cardiopulmonary bypass (CPB), neutrophils become activated due to contact with extracorporeal surfaces and binding of complement fragments C3a and C5a, leading to extravasation and subsequent tissue damage. In this study, the effects of the leumedin NPC 15669 (N [9H - (2,7 dimethylfluorenyl - 9 - methoxy) car bonyl]-L-leucine), a leukocyte recruitment inhibitor, were evaluated in a pig model of CPB. NPC 15669 caused significant inhibition of CPB associated increase in CD18 upregulation, lung tissue myeloperoxidase content, and percentage wet weight compared to controls. Lung histology revealed clear airways and minimal neutrophil infiltration in treated animals vs. significant oedema and cellular infiltration in controls. It is concluded that CPB causes a dramatic increase in neutrophil CD18, and that leumedins are effective in inhibiting neutrophil activation and subsequent tissue injury when administered during CPB. |
Databáze: | OpenAIRE |
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