| Popis: |
Since the first report of Northover and Subramanian [1] in 1962 on the use of aspirin to prevent death due to endotoxin shock in mongrel dogs, there has been a near-continuous stream of investigations the results of which support the potential for cyclooxygenase inhibition in sepsis syndrome. Many of these studies are survival studies, i.e., intervention with cyclooxygenase inhibitors is intended to determine effects on mortality. It is clear from these data that treatment with inhibitors of cyclooxygenase improves survival, though the biochemical and physiological mechanisms responsible for this beneficial effect have not been well understood until recently [2–8]. With the discovery of arachidonic acid and its metabolites, which include prostaglandins, thromboxanes, and leukotrienes, interpretations of the physiologic effects of cyclooxygenase inhibition have been attributed to key metabolites of arachidonic acid [5, 6]. In the past 15 years data have become available linking abnormalities of prostaglandin metabolism with airway mechanics abnormalities, pulmonary hypertension and the associated hypoxemia, cardiovascular collapse, and multiple organ system failure [6–14]. |
