Infection remains a major cause of death in patients suffering trauma. Such patients have also been demonstrated to have elevated levels of thromboxane. We evaluated the effect of elevated levels of thromboxane on resistance to sepsis using a long-acting thromboxane analogue in multiple experimental models. The thromboxane analogue was found to have no effect on the percentage distribution of T cell subsets or on the percentage of T cells bearing interleukin-2 or transferrin receptors. The thromboxane analogue did not alter mortality rates in the Pseudomonas burn wound infection model. However, the analogue was found to increase leukocyte infiltration of burn wounds and increase mortality in both an Escherichia coli peritonitis model and a heat-killed Escherichia coli intravenous endotoxin model. The etiology of this apparent discrepancy of improved immune function and decreased survival in septic models may be the result of either a hyperimmune response which results in tissue damage or the hemodynamic effect of thromboxane.
|Idioma original||English (US)|
|Número de páginas||8|
|Publicación||Surgical Research Communications|
|Estado||Published - ene 1 1991|
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