Mediators of multiple organ failure
Author:
- 1 March 1990
- journal article
- review article
- Published by Springer Nature in Intensive Care Medicine
- Vol. 16 (S3) , S192-S196
Abstract
Multiple Organ Failure (MOF) has largely been attributed to bacterial sepsis, though conclusive evidence of an essential role for bacteria and/or their endotoxins is still lacking. On the other hand, MOF and the clinical syndrome of sepsis may be aseptically induced in germfree animals. This paper reviews the evidence that excessive activation of endogenous humoral mediators and inflammatory cells may cause this highly lethal syndrome.Keywords
This publication has 49 references indexed in Scilit:
- Tumor Necrosis Factor and Interleuktn-1 in the Serum of Children with Severe Infectious PurpuraNew England Journal of Medicine, 1988
- Interleukin 1 induces a shock-like state in rabbits. Synergism with tumor necrosis factor and the effect of cyclooxygenase inhibition.Journal of Clinical Investigation, 1988
- Complement Depletion in a Porcine Model of Septic Acute Respiratory Disease1987
- Secretory products of macrophages.Journal of Clinical Investigation, 1987
- Neopterin heute*DMW - Deutsche Medizinische Wochenschrift, 1987
- Shock and Tissue Injury Induced by Recombinant Human CachectinScience, 1986
- Cachectin and tumour necrosis factor as two sides of the same biological coinNature, 1986
- Neutrophil-mediated injury to endothelial cells. Enhancement by endotoxin and essential role of neutrophil elastase.Journal of Clinical Investigation, 1986
- The Role of C5 in Septic Lung InjuryAnnals of Surgery, 1985
- Interleukin-1Clinical Infectious Diseases, 1984