Prostaglandins, cyclo-oxygenase inhibitors, and thromboxane synthetase inhibitors in the pathogenesis of multiple systems organ failure.

The role of the various cyclo-oxygenase products of arachidonic acid metabolism in the production of the pathologic, physiologic, hemodynamic, and metabolic derangements of sepsis has been reviewed and there is a wide variation in different species and with different models of sepsis. The relationship of these potential mediators cannot be definitely determined. There is much circumstantial evidence that would incriminate the various arachidonic metabolites in the production of the sepsis manifestations; however, we must keep in mind that this may only be "guilt by association." Clearly, the available evidence does suggest that there is some role played by TXA2 and PGI2 in the physiologic and hemodynamic manifestations of sepsis, but the exact role remains undetermined.