The effect of aprotinin on hypoxia-reoxygenation-induced changes in neutrophil and endothelial function.

Hdl Handle:
http://hdl.handle.net/10147/208923
Title:
The effect of aprotinin on hypoxia-reoxygenation-induced changes in neutrophil and endothelial function.
Authors:
Harmon, D; Lan, W; Shorten, G
Affiliation:
Cork University Hospital, Department of Anaesthesia and Intensive Care Medicine, , Cork, Ireland. dharmon@indigo.ie
Citation:
Eur J Anaesthesiol. 2004 Dec;21(12):973-9.
Journal:
European journal of anaesthesiology
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/208923
PubMed ID:
15719861
Abstract:
BACKGROUND AND OBJECTIVE: An acute inflammatory response associated with cerebral ischaemia-reperfusion contributes to the development of brain injury. Aprotinin has potential, though unexplained, neuroprotective effects in patients undergoing cardiac surgery. METHODS: Human neutrophil CD11 b/CD18, endothelial cell intercellular adhesion molecule-1 (ICAM-1) expression and endothelial interleukin (IL)-1beta supernatant concentrations in response to in vitro hypoxia-reoxygenation was studied in the presence or absence of aprotinin (1600 KIU mL(-1)). Adhesion molecule expression was quantified using flow cytometry and IL-1beta concentrations by enzyme-linked immunosorbent assay. Data were analysed using ANOVA and post hoc Student-Newman-Keuls test as appropriate. RESULTS: Exposure to 60-min hypoxia increased neutrophil CD11b expression compared to normoxia (170+/-46% vs. 91+/-27%, P = 0.001) (percent intensity of fluorescence compared to time 0) (n = 8). Hypoxia (60 min) produced greater upregulation of CD11b expression in controls compared to aprotinin-treated neutrophils [(170+/-46% vs. 129+/-40%) (P = 0.04)] (n = 8). Hypoxia-reoxygenation increased endothelial cell ICAM-1 expression (155+/-3.7 vs. 43+/-21 mean channel fluorescence, P = 0.0003) and IL-1beta supernatant concentrations compared to normoxia (3.4+/-0.4 vs. 2.6+/-0.2, P = 0.02) (n = 3). Hypoxia-reoxygenation produced greater upregulation of ICAM- 1 expression [(155+/-3.3 vs. 116+/-0.7) (P = 0.001)] and IL-1beta supernatant concentrations [(3.4+/-0.3 vs. 2.6+/-0.1) (P = 0.01)] in controls compared to aprotinin-treated endothelial cell preparation (n = 3). CONCLUSIONS: Hypoxia-reoxygenation-induced upregulation of neutrophil CD11b, endothelial cell ICAM-1 expression and IL-1beta concentrations is decreased by aprotinin at clinically relevant concentrations.
Language:
eng
MeSH:
Analysis of Variance; Aprotinin/*pharmacology; Brain Ischemia/*metabolism; Cell Adhesion/drug effects/physiology; Cell Adhesion Molecules/drug effects/metabolism; Cells, Cultured; Endothelium, Vascular/*drug effects/metabolism; Enzyme-Linked Immunosorbent Assay/methods; Flow Cytometry/methods; Hemostatics/*pharmacology; Humans; Intercellular Adhesion Molecule-1/drug effects/metabolism; Interleukin-1/metabolism; Neutrophils/*drug effects/metabolism; Reference Values; Reperfusion/methods; Reperfusion Injury/metabolism; Time Factors; Umbilical Veins
ISSN:
0265-0215 (Print); 0265-0215 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorHarmon, Den_GB
dc.contributor.authorLan, Wen_GB
dc.contributor.authorShorten, Gen_GB
dc.date.accessioned2012-02-03T15:07:32Z-
dc.date.available2012-02-03T15:07:32Z-
dc.date.issued2012-02-03T15:07:32Z-
dc.identifier.citationEur J Anaesthesiol. 2004 Dec;21(12):973-9.en_GB
dc.identifier.issn0265-0215 (Print)en_GB
dc.identifier.issn0265-0215 (Linking)en_GB
dc.identifier.pmid15719861en_GB
dc.identifier.urihttp://hdl.handle.net/10147/208923-
dc.description.abstractBACKGROUND AND OBJECTIVE: An acute inflammatory response associated with cerebral ischaemia-reperfusion contributes to the development of brain injury. Aprotinin has potential, though unexplained, neuroprotective effects in patients undergoing cardiac surgery. METHODS: Human neutrophil CD11 b/CD18, endothelial cell intercellular adhesion molecule-1 (ICAM-1) expression and endothelial interleukin (IL)-1beta supernatant concentrations in response to in vitro hypoxia-reoxygenation was studied in the presence or absence of aprotinin (1600 KIU mL(-1)). Adhesion molecule expression was quantified using flow cytometry and IL-1beta concentrations by enzyme-linked immunosorbent assay. Data were analysed using ANOVA and post hoc Student-Newman-Keuls test as appropriate. RESULTS: Exposure to 60-min hypoxia increased neutrophil CD11b expression compared to normoxia (170+/-46% vs. 91+/-27%, P = 0.001) (percent intensity of fluorescence compared to time 0) (n = 8). Hypoxia (60 min) produced greater upregulation of CD11b expression in controls compared to aprotinin-treated neutrophils [(170+/-46% vs. 129+/-40%) (P = 0.04)] (n = 8). Hypoxia-reoxygenation increased endothelial cell ICAM-1 expression (155+/-3.7 vs. 43+/-21 mean channel fluorescence, P = 0.0003) and IL-1beta supernatant concentrations compared to normoxia (3.4+/-0.4 vs. 2.6+/-0.2, P = 0.02) (n = 3). Hypoxia-reoxygenation produced greater upregulation of ICAM- 1 expression [(155+/-3.3 vs. 116+/-0.7) (P = 0.001)] and IL-1beta supernatant concentrations [(3.4+/-0.3 vs. 2.6+/-0.1) (P = 0.01)] in controls compared to aprotinin-treated endothelial cell preparation (n = 3). CONCLUSIONS: Hypoxia-reoxygenation-induced upregulation of neutrophil CD11b, endothelial cell ICAM-1 expression and IL-1beta concentrations is decreased by aprotinin at clinically relevant concentrations.en_GB
dc.language.isoengen_GB
dc.subject.meshAnalysis of Varianceen_GB
dc.subject.meshAprotinin/*pharmacologyen_GB
dc.subject.meshBrain Ischemia/*metabolismen_GB
dc.subject.meshCell Adhesion/drug effects/physiologyen_GB
dc.subject.meshCell Adhesion Molecules/drug effects/metabolismen_GB
dc.subject.meshCells, Cultureden_GB
dc.subject.meshEndothelium, Vascular/*drug effects/metabolismen_GB
dc.subject.meshEnzyme-Linked Immunosorbent Assay/methodsen_GB
dc.subject.meshFlow Cytometry/methodsen_GB
dc.subject.meshHemostatics/*pharmacologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIntercellular Adhesion Molecule-1/drug effects/metabolismen_GB
dc.subject.meshInterleukin-1/metabolismen_GB
dc.subject.meshNeutrophils/*drug effects/metabolismen_GB
dc.subject.meshReference Valuesen_GB
dc.subject.meshReperfusion/methodsen_GB
dc.subject.meshReperfusion Injury/metabolismen_GB
dc.subject.meshTime Factorsen_GB
dc.subject.meshUmbilical Veinsen_GB
dc.titleThe effect of aprotinin on hypoxia-reoxygenation-induced changes in neutrophil and endothelial function.en_GB
dc.contributor.departmentCork University Hospital, Department of Anaesthesia and Intensive Care Medicine, , Cork, Ireland. dharmon@indigo.ieen_GB
dc.identifier.journalEuropean journal of anaesthesiologyen_GB
dc.description.provinceMunster-
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