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Dabby D, Greif F, Yaniv M, Rubin M, Dekel S, Lelcuk S. Thromboxane A2 in Postischemic Acute Compartmental Syndrome. Arch Surg. 1998;133(9):953–956. doi:10.1001/archsurg.133.9.953
To evaluate whether thromboxane A2 participates in the ischemia-reperfusion injury associated with acute compartmental syndrome (ACS) and if by using a cyclooxygenase inhibitor this can be either reduced or abolished.
To assess the role of thromboxane A2 in ACS, a tourniquet was applied for 2 hours to the hind limb of 12 dogs. Group 1 (n=6) served as controls while group 2 (n=6) was pretreated with lysine-acetyl-salicylate (Lysoprim). Blood thromboxane B2 levels and intracompartmental pressures were assayed prior to inflation of the tourniquet and at 5 minutes, 90 minutes, and 24, 72, and 144 hours after deflation.
Five minutes after deflation, the compartmental pressure increased from 11.2±2.2 mm Hg to 16.1±3.3 mm Hg and 17±2.2 mm Hg (mean±SD) in groups 2 and 1, respectively. At 90 minutes and 24 hours, pressures were 17.1±3.3 mm Hg and 23.2±3.3 mm Hg (P<.01) and 15.3±2.6 mm Hg and 25.2±1.8 mm Hg (mean±SD) (P<.001), respectively, in groups 2 and 1. A similar effect, although of a lesser magnitude, was observed in the counterlateral limb. Thromboxane B2 levels increased from a mean (±SD) of 46±5.5 pg/0.1mL to 132±7.5 pg/0.1 mL at 90 minutes in group 1, while remaining unchanged in group 2.
Thromboxane A2 plays a major role in the ischemia-reperfusion injury of acute compartmental syndrome. By using a cyclooxygenase inhibitor both the levels of thromboxane and the compartmental pressures can be reduced.
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