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Thromboxane A2 in Postischemic Acute Compartmental Syndrome
Dan Dabby, MD;
Franklin Greif, MD, FACS;
Moshe Yaniv, MD;
Moshe Rubin, MD;
Shmuel Dekel, MD;
Shlomo Lelcuk, MD
Arch Surg. 1998;133:953-956.
Objective 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.
Design 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.
Results 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.
Conclusions 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.
From the Departments of Surgery B, The Rabin Medical Center (Beilinson Campus) (Drs Greif, Rabin, and Lelcuk) and Orthopedics B, The Sourasky Medical Center (Drs Dabby, Yaniv, and Dekel), Petah-Tikva, Israel, and The Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
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