Pentoxifylline Interferes with Potental Sources of Free Radical Generation during Endotoxemia
Increased concentrations of tumor necrosis factor concentrations, activated neutrophils, and inadequate oxygen delivery to tissue are associated with free radical generation and also with endotoxic shock. Pentoxifylline suppresses the synthesis of tumor necrosis factor in endotoxin stimulated macrophages1 and when administered in vivo significantly attenuates circulating tumor necrosis factor and survival in mice challenged with endotoxin.2 Pentoxifylline also inhibits neutrophil activation induced by tumor necrosis factor.3 Additionally, pentoxifylline possesses antithrombotic activity and induces synthesis of endothelial cell prostacyclin, both of which should promote tissue perfusion during endotoxin-induced low flow conditions. This study was designed to determine the effect of pentoxifylline on the development of cardiovascular, metabolic, and pathologic responses to endotoxin.
KeywordsTumor Necrosis Factor Free Radical Generation Endotoxic Shock Center 3Veterans Affair Medical Antithrombotic Activity
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