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Chest, Vol 87, 726-730, Copyright © 1985 by American College of Chest Physicians
ARTICLES |
M Leeman, JM Boeynaems, JP Degaute, JL Vincent and RJ Kahn
Experimental studies suggest that thromboxane A2 could play a role in the pulmonary hypertension of the adult respiratory distress syndrome (ARDS). We therefore investigated the hemodynamic and gasometric effects of dazoxiben, a selective thromboxane synthetase inhibitor, in seven patients who had developed ARDS. The patients were studied for 120 minutes after a single intravenous bolus of 1.5 mg of dazoxiben per kilogram of body weight. During this period, there was no change in pulmonary hemodynamics, a moderate increase in arterial oxygen pressure, and a slight decrease in venous admixture. Therefore, administration of dazoxiben in patients with ARDS does not decrease pulmonary hypertension. This study does not support the role of thromboxane A2 as an important mediator in pulmonary hypertension in human ARDS, at least once the syndrome has been recognized.
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