ABSTRACT
Numerous animal studies in a variety of species have focused on the demonstration of elevated serum platelet-activating factor (PAF) levels in sepsis. Initial studies aimed at defining a role for PAF in sepsis were based on the demonstration that PAF infusion produced hypotension and death in a variety of species. PAF’s ability to increase one of the hallmark indexes of human sepsis, microvascular permeability, has been widely documented. Studies utilizing highly specific PAF antagonists that have demonstrated significant protective effects are another line of evidence that support the involvement of PAF in the pathophysiology of sepsis. A careful review of the accuracy, validity, and reproducibility of methods employed to measure PAF in sepsis suggest that while they appear convincing, they in fact need much improvement. The majority of PAF measurements were performed by functional bioassays such as platelet-serotonin release and platelet aggregation. Data derived from clinical studies in support of PAF’s role in the development of sepsis are scarce.
