Differential secretion of prostaglandin E(2), thromboxane A(2) and interleukin-6 in intact and ruptured abdominal aortic aneurysms.

Ruptured abdominal aortic aneurysm (AAA) contributes largely to aneurysm-related morbidity and mortality. An inflammatory gene, COX-2, was found to be widely expressed in AAA. However, the involvement of COX-2 metabolites and other inflammatory mediators in the disease and particularly in AAA rupture still needs elucidation. The purpose of the present study was to evaluate the secretion of inflammatory mediators and the expression of macrophages in aneurysms and determine their significance in ruptured AAA. Aortic tissue was harvested at time of aortic reconstructive surgery for the group of intact AAA (n=20) and ruptured AAA (n=10) or at time of organ harvest for normal aortic tissue (n=4). Aortic explant cultures were immediately established and the culture medium was collected after 72 h. Specific enzyme-linked immunoassorbent assays were used to quantify COX-2 metabolites and inflammatory cytokines. Inflammatory macrophage cells were also quantified in the corresponding aortic walls immunohistochemically. Differences in the secretory levels of inflammatory metabolites and the macrophage quantity in all groups were assessed. All three explant culture groups secreted detectable levels of studied COX-2 metabolites, including PGE(2), PGF(2alpha), PGI(2) and TxB(2) and inflammatory cytokines, including interleukin (IL)-1beta, IL-6, IL-8 and IL-10. The secretory levels of PGE(2), TXB(2) and IL-6 were highest in the ruptured AAA explant cultures and statistically higher than those in intact AAA cultures (p<0.05). The secretion of those inflammatory mediators and the local expression of macrophages in ruptured aneurysm probably reflects the active inflammatory processes in the aortic lesions. A means of modifying the inflammatory process in the wall of AAAs might play an important role in preventing aneurysm rupture.