Hyperphospholipasemia A2 in human volunteers challenged with intravenous endotoxin
| Autor: | J. Browning, Eva Stefanski, B. Sternby, Peter Vadas, Anthony F. Suffredini, D. W. Wilmore, Waldemar Pruzanski, A. G. D. Hoffman, G. D. Martich |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
medicine.medical_specialty
Immunology Inflammation Phospholipases A Pentoxifylline chemistry.chemical_compound Immune system Phospholipase A2 Reference Values Internal medicine medicine Humans Immunology and Allergy Infusions Intravenous Neutralizing antibody biology Tumor Necrosis Factor-alpha business.industry Ibuprofen Endotoxins Phospholipases A2 Endocrinology chemistry biology.protein lipids (amino acids peptides and proteins) Tumor necrosis factor alpha Lysozyme medicine.symptom business medicine.drug |
| Zdroj: | Inflammation. 16:561-570 |
| ISSN: | 1573-2576 0360-3997 |
| Popis: | Phospholipase A2 (PLA2) activity was measured in the serum of 23 individuals infused intravenously with endotoxin (EN) at a dose of 4 ng/kg body weight. A marked increase in PLA2 was noted 3 h after EN challenge (mean 828 +/- 513 units/ml), reached its maximum at 24 h after the challenge (mean 2667 +/- 2442 units/ml), and was still evident at 48 h (mean 763 +/- 366 units/ml). In contrast, TNF levels were maximal (mean 712 +/- 375 pg/ml) 90 min after the EN challenge and subsided to very low values (5 +/- 5 pg/ml) 5 h after the challenge. There was a positive correlation between the maximum response of TNF and that of PLA2 (r = 0.82, P0.01). Administration of ibuprofen or pentoxifylline did not alter the PLA2 response. EN challenge did not affect serum pancreatic PLA2 concentration or that of the lysosomal cationic enzyme, lysozyme. Neutralizing antibody against human recombinant (synovial type) PLA2 completely abolished PLA2 activity in the sera tested. We conclude that EN infusions cause marked intravascular release of nonpancreatic secretory PLA2 and that the magnitude of this response seems to be related to the prior generation of TNF. |
| Databáze: | OpenAIRE |
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