Answer: d Inflammatory mediators have recently been recognized as playing a significant role in the clinical manifestations and progression of shock and the development of subsequent complications. These mediator systems function primarily as parcrine and autocrine agents in the local environment and are not usually detectable systemically. The over-expression and systemic dissemination of these mediators produces the toxic autodestructive processes underlying multiorgan failure syndrome with attendant high mortality. The compliment cascade is activated in shock and tissue injury through both the classical and alternative pathways. Activation of either pathway results in generation of the anaphylatoxin, C3a and C5a, soluble products with potent systemic hemodynamic effects. The eicosanoids, which include the prostaglandins and leukotrienes are formed acutely from arachidonic acid released from the membrane phospholipid by phospholipase A2. Eicosanoids are not stored in any measurable level and are generated as needed from readily available arachidonic acid in response to various inflammatory phenomena. Platelets, white cells, and endothelial cells are a rich source of these compounds. Thromboxane (TXA2) is the major arachidonic acid metabolite elaborated by platelets. TXA2 induces intense vasoconstriction, platelet aggregation and degranulation, neutrophil margination in the microcirculation and bronchial constriction. PGI2, the major arachidonic acid metabolite formed by endothelial cells, serves a check against actions of TXA2. PGI2 is a vasodilator and a potent inhibitor of platelet aggregation. Platelet aggravating factor is a potent phospholipid mediator released by neutrophils, platelets, macrophages and endothelial cells in response to ischemia, tissue injury and sepsis. Its effects include decreased cardiac function, increased pulmonary vascular resistance, bronchoconstriction, peripheral vasodilatation, and increased vascular permeability