Thromboxane A2 in postischemic acute compartmental syndrome

Dan Dabby, Franklin Greif*, Moshe Yaniv, Moshe Rubin, Shmuel Dekel, Shlomo Lelcuk

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

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/0.1 mL 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.

Original languageEnglish
Pages (from-to)953-956
Number of pages4
JournalArchives of Surgery
Volume133
Issue number9
DOIs
StatePublished - Sep 1998

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