Tourniquet-induced systemic inflammatory response in extremity surgery.
Affiliation
Department of Academic Surgery, Cork University Hospital, Cork, Ireland.Issue Date
2012-02-03T15:11:08ZMeSH
AdultAnalysis of Variance
Antigens, CD11/blood
Antigens, CD14/blood
*Arthroplasty, Replacement, Knee
Cell Migration Inhibition
Cells, Cultured
Cytokines/blood
Female
Humans
Male
Neutrophils/immunology
Prospective Studies
Reperfusion Injury/blood/*complications
Systemic Inflammatory Response Syndrome/blood/*etiology
Tourniquets/*adverse effects
Metadata
Show full item recordCitation
J Trauma. 2001 Nov;51(5):922-6.Journal
The Journal of traumaPubMed ID
11706341Abstract
BACKGROUND: 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. METHODS: 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-alpha, interleukin (IL)-1beta, and IL-10 were also determined. RESULTS: 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-alpha and IL-1beta 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. CONCLUSION: These results indicate a transient neutrophil and monocyte activation after tourniquet-ischemia that translates into enhanced neutrophil transendothelial migration with potential for tissue injury.Language
engISSN
0022-5282 (Print)0022-5282 (Linking)
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