Since the initial discovery of the leukotrienes by Samuelsson and co-workers 1 , 2 and the subsequent characterization of their biological effects, these enzymatic products of the 5-lipoxygenase pathway have been the subject of intense research interest. The leukotrienes are derived initially from the oxidative metabolism of arachidonic acid through the 5-lipoxygenase pathway (Figure 1). Leukotriene (LT)C4, LTD4, and LTE4, often referred to as the peptidoleukotrienes or cysteinyl leukotrienes because their formation is initiated by the adduct of LTA4 with glutathione, are produced by a variety of cell types including macrophages, mast cells, peritoneal leukocytes, pulmonary parenchymal cells, and vascular smooth muscle cells. 12 Alternatively, LTA4 can be metabolized to LTB4, which is not one of the peptidoleukotrienes. The leukotrienes have been ascribed to be potent mediators of inflammatory and anaphylactic responses, 3 , 4 and produce several of the pathophysiologic responses noted to occur in endotoxemia or septicemia. These effects include decreased cardiac output, increased systemic vascular resistance, increased microvascular permeability, and leukopenia secondary to increased adherence to the endothelial lining of the microvasculature (Table 1). Bacterial lipopolysaccharides (LPS) stimulate the formation of 5-lipox-ygenase products, 5-8 although the circulating levels of many other humoral substances implicated as contributing to the consequences of circulatory shock are also enhanced as a consequence of endotoxemia.