Intestinal reperfusion (IR)-induced pulmonary edema has been related to endogenous pulmonary thromboxane A2 (TxA2) release. This study examines the hypothesis that alveolar macrophages (aMφs) activated during IR are an important cellular source of TxA2 in this model. Anesthetized Sprague Dawley rats underwent 120 min of intestinal ischemia and 60 min of reperfusion (IR) or sham operation (Sham). aMφs were isolated by bronchoalveolar lavage and incubated in Krebs buffer for 30 min, after which the supernatant was analyzed for TxB2 (metabolite of TxA2) and prostaglandin E2. Other parameters of aMφ activation measured included lysosomal enzyme release (β-glucuronidase), superoxide (O2-) release, and procoagulant activity. aMφs from animals sustaining IR generated more than twice as much TxA2 and prostaglandin E2 as did those isolated from controls (p < .05). Other evidence of aMφ activation included a nearly 100-fold increase in procoagulant activity, a 7-fold increase in β-glucuronidase release, and a 2.5-fold increase in O2 release over that of controls (p < .05). These data suggest that TxA2 is a major eicosanoid product of aMφs during IR and that aMφs may be an important cellular participant in IR-induced pulmonary microvascular injury, either directly by releasing O2-, lysosomal enzymes, and pro-coagulant factors, or indirectly by generating TxA2.