Tourniquet-induced systemic inflammatory response in extremity surgery.

Hdl Handle:
http://hdl.handle.net/10147/209058
Title:
Tourniquet-induced systemic inflammatory response in extremity surgery.
Authors:
Wakai, A; Wang, J H; Winter, D C; Street, J T; O'Sullivan, R G; Redmond, H P
Affiliation:
Department of Academic Surgery, Cork University Hospital, Cork, Ireland.
Citation:
J Trauma. 2001 Nov;51(5):922-6.
Journal:
The Journal of trauma
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/209058
PubMed ID:
11706341
Abstract:
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:
eng
MeSH:
Adult; Analysis 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
ISSN:
0022-5282 (Print); 0022-5282 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorWakai, Aen_GB
dc.contributor.authorWang, J Hen_GB
dc.contributor.authorWinter, D Cen_GB
dc.contributor.authorStreet, J Ten_GB
dc.contributor.authorO'Sullivan, R Gen_GB
dc.contributor.authorRedmond, H Pen_GB
dc.date.accessioned2012-02-03T15:11:08Z-
dc.date.available2012-02-03T15:11:08Z-
dc.date.issued2012-02-03T15:11:08Z-
dc.identifier.citationJ Trauma. 2001 Nov;51(5):922-6.en_GB
dc.identifier.issn0022-5282 (Print)en_GB
dc.identifier.issn0022-5282 (Linking)en_GB
dc.identifier.pmid11706341en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209058-
dc.description.abstractBACKGROUND: 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.en_GB
dc.language.isoengen_GB
dc.subject.meshAdulten_GB
dc.subject.meshAnalysis of Varianceen_GB
dc.subject.meshAntigens, CD11/blooden_GB
dc.subject.meshAntigens, CD14/blooden_GB
dc.subject.mesh*Arthroplasty, Replacement, Kneeen_GB
dc.subject.meshCell Migration Inhibitionen_GB
dc.subject.meshCells, Cultureden_GB
dc.subject.meshCytokines/blooden_GB
dc.subject.meshFemaleen_GB
dc.subject.meshHumansen_GB
dc.subject.meshMaleen_GB
dc.subject.meshNeutrophils/immunologyen_GB
dc.subject.meshProspective Studiesen_GB
dc.subject.meshReperfusion Injury/blood/*complicationsen_GB
dc.subject.meshSystemic Inflammatory Response Syndrome/blood/*etiologyen_GB
dc.subject.meshTourniquets/*adverse effectsen_GB
dc.titleTourniquet-induced systemic inflammatory response in extremity surgery.en_GB
dc.contributor.departmentDepartment of Academic Surgery, Cork University Hospital, Cork, Ireland.en_GB
dc.identifier.journalThe Journal of traumaen_GB
dc.description.provinceMunster-

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