Bernice L Y Cheuk1, Stephen W K Cheng. 1. Department of Surgery, The University of Hong Kong, 14/F, South Wing, Block K, Queen Mary Hospital, 102 Pofkulam, Hong Kong, HKSAR, 852, Hong Kong.
Abstract
BACKGROUND: Our laboratory has previously shown that the levels of secreted prostaglandin E(2) (PGE(2)), Thromboxane B(2) (TxB(2)), and interleukin-6 (IL-6) by aortic explant cultures were high in patients with ruptured abdominal aortic aneurysm (AAA). In the present study, we sought to examine the secretory levels of these inflammatory mediators in aortic explant cultured from a group of AAAs rupturing at a certain size and a group that did not rupture at that size. It was thought that such a comparison might reveal the contribution of those inflammatory mediators to the risk of AAA rupture. MATERIALS AND METHODS: All subjects had abdominal computed tomography (CT) scans to determine the size of the aneurysm, and surgical aortic tissue was collected from both nonruptured AAAs (18 with a mean size of 6 + 0.5 cm [range: 5-7 cm] and 12 with a mean size of 8 + 0.1 cm [range: 7.01-10 cm]) and ruptured AAAs (10 with a mean size of 5.8 + 0.3 cm [range: 5-7 cm] and 10 with a mean size of 7.8 + 0.1 cm [range: 7.01-10 cm]). Aortic explant cultures from different sizes of aneurysms were immediately established and the culture media were collected 72 h later. RESULTS: The levels of PGE(2), TxB(2), and IL-6 secreted in the cultured medium were quantified by specific enzyme-linked immunosorbent assays (ELISA). The secretary levels of PGE(2), TxB(2), and IL-6 were significantly higher in ruptured AAAs than in nonruptured AAAs of similar diameter. However, there was no correlation between these three inflammatory mediators and the size of AAA. CONCLUSIONS: This study shows that these inflammatory mediators may play a role in the progression toward rupture but may not be responsible for the expansion of AAA.
BACKGROUND: Our laboratory has previously shown that the levels of secreted prostaglandin E(2) (PGE(2)), Thromboxane B(2) (TxB(2)), and interleukin-6 (IL-6) by aortic explant cultures were high in patients with ruptured abdominal aortic aneurysm (AAA). In the present study, we sought to examine the secretory levels of these inflammatory mediators in aortic explant cultured from a group of AAAs rupturing at a certain size and a group that did not rupture at that size. It was thought that such a comparison might reveal the contribution of those inflammatory mediators to the risk of AAA rupture. MATERIALS AND METHODS: All subjects had abdominal computed tomography (CT) scans to determine the size of the aneurysm, and surgical aortic tissue was collected from both nonruptured AAAs (18 with a mean size of 6 + 0.5 cm [range: 5-7 cm] and 12 with a mean size of 8 + 0.1 cm [range: 7.01-10 cm]) and ruptured AAAs (10 with a mean size of 5.8 + 0.3 cm [range: 5-7 cm] and 10 with a mean size of 7.8 + 0.1 cm [range: 7.01-10 cm]). Aortic explant cultures from different sizes of aneurysms were immediately established and the culture media were collected 72 h later. RESULTS: The levels of PGE(2), TxB(2), and IL-6 secreted in the cultured medium were quantified by specific enzyme-linked immunosorbent assays (ELISA). The secretary levels of PGE(2), TxB(2), and IL-6 were significantly higher in ruptured AAAs than in nonruptured AAAs of similar diameter. However, there was no correlation between these three inflammatory mediators and the size of AAA. CONCLUSIONS: This study shows that these inflammatory mediators may play a role in the progression toward rupture but may not be responsible for the expansion of AAA.
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