The Journal of Trauma: Injury, Infection, and Critical Care. 51(5):922-926, NOVEMBER 2001
PMID: 11706341
Issn Print: 0022-5282
Publication Date: November 2001
Tourniquet-Induced Systemic Inflammatory Response in Extremity Surgery
Abel Wakai;Jiang Wang;Desmond Winter;John Street;Ronan O’Sullivan;Henry Redmond;
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From the Departments of Academic Surgery (A.W., J.H.W., J.T.S., R.G.O., H.P.R.) and General Surgery (D.C.W.), Cork University Hospital, Cork, Ireland.
Abstract
Tourniquet-induced reperfusion injury in animals produces significant systemic inflammatory effects. This study investigated whether a biologic response occurs in a clinically relevant model of tourniquet-induced reperfusion injury.Patients undergoing elective knee arthroscopy were prospectively randomized into controls (no tourniquet) and subjects (tourniquet-controlled). The effects of tourniquet-induced reperfusion on monocyte activation state, neutrophil activation state, and transendothelial migration (TEM) were studied. Changes in the cytokines implicated in reperfusion injury, tumor necrosis factor-α, interleukin (IL)-1β, and IL-10 were also determined.After 15 minutes of reperfusion, neutrophil and monocyte activation were significantly increased. Pretreatment of neutrophils with pooled subject (ischemia-primed) plasma significantly increased TEM. In contrast, TEM was not significantly altered by ischemia-primed plasma pretreatment of the endothelial monolayer. Significant elevation of tumor necrosis factor-α and IL-1β were observed in subjects compared with controls after 15 minutes of reperfusion. There was no significant difference in serum IL-10 levels between the groups at all the time points studied.These results indicate a transient neutrophil and monocyte activation after tourniquet-ischemia that translates into enhanced neutrophil transendothelial migration with potential for tissue injury.
