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Abstract:
The Adult Respiratory Distress Syndrome (ARDS) is characterized by high- permeability pulmonary oedema containing plasma-derived proteins, decreased lung volumes, decreased compliance, and arterial hypoxaemia. ARDS results from a number of different causes, of which Gram-negative sepsis and endotoxin (lipopolysaccharide, LPS) from bacteria and aspiration are thought to be major causes to the development of this life-threatening syndrome (1, 2). Although insight into the clinical course of ARDS patients is increasing, the sequence of pathophysiological events remains poorly understood (3, 4, 5). Currently, it is becoming widely accepted that an inflammatory reaction occurs in the lungs, in which numerous cellular and humoral mechanisms are involved, including macrophages, neutrophils, platelets, coagulation and fibrinolytic systems (6). Activated alveolar macrophages (AM) may contribute to this inflammatory reaction by the in vivo production of reactive oxygen intermediates (ROl) and chemotactic cytokines, of which TNFct seems to be the major one (7, 8, 9). Some of the damage done by ROl in vivo is assumed to be due to hydroxyl radicals (OH) (10, 11) that emerge from the conversion of O2 and H2O2. Not only in vivo experiments were in favour of a potential role for TNFct in pulmonary damage (12), but also in vitro experiments supported these findings (13, 14). In vitro TNFct was capable of 'priming' PMNs for secondary stimuli (15, 16, 17). In addition to the central role of ROl and TNFct, there is clear support for the involvement of a multimediator network that leads to lung tissue injury (18). During the development of ARDS, the generation of various mediators contribute to the development of severe lung damage.
| Description: |
Final rept. |
| Pages: |
34 |
| Report Date: |
AUG 96 |
| Report Number: |
A336513 |
Report Unavailable |
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