Intestinal reperfusion (IR)-induced pulmonary edema has been related t
o endogenous pulmonary thromboxane A(2) (TxA(2)) release. This study e
xamines the hypothesis that alveolar macrophages (aM phi s) activated
during IR are an important cellular source of TxA(2) in this model. An
esthetized Sprague Dawley rats underwent 120 min of intestinal ischemi
a and 60 min of reperfusion (IR) or sham operation (Sham). aM phi s we
re isolated by bronchoalveolar lavage and incubated in Krebs buffer fo
r 30 min, after which the supernatant was analyzed for TxB(2) (metabol
ite of TxA(2)) and prostaglandin E-2. Other parameters of aM phi activ
ation measured included lysosomal enzyme release (beta-glucuronidase),
superoxide (O-2(-)) release, and procoagulant activity, aM phi s from
animals sustaining IR generated more than twice as much TxA(2) and pr
ostaglandin E-2 as did those isolated from controls (p <.05). Other ev
idence of aM phi activation included a nearly 100-fold increase in pro
coagulant activity, a 7-fold increase in beta-glucuronidase release, a
nd a 2.5-fold increase in O-2(-) release over that of controls (p <.05
). These data suggest that TxA(2) is a major eicosanoid product of aM
phi s during IR and that aM phi s may be an important cellular partici
pant in IR-induced pulmonary microvascular injury, either directly by
releasing O-2(-), lysosomal enzymes, and pro-coagulant factors, or ind
irectly by generating TxA(2).