Impact of the neutrophil response to granulocyte colony-stimulating factor on the risk of hemorrhage when used in combination with tissue plasminogen activator during the acute phase of experimental stroke

Granulocyte colony-stimulating factor (G-CSF) is a pharmacologic agent inducing neutrophil mobilization and a new candidate for neuroprotection and neuroregeneration in stroke. Its effects when used in combination with tissue plasminogen activator (tPA) were explored during the acute phase of ischem...

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Bibliographic Details
Published in:Journal of neuroinflammation 2014-05, Vol.11 (1), p.96-96
Main Authors: Gautier, Sophie, Ouk, Thavarak, Tagzirt, Madjid, Lefebvre, Catherine, Laprais, Maud, Pétrault, Olivier, Dupont, Annabelle, Leys, Didier, Bordet, Régis
Format: Article
Language:English
Subjects:
Animals
Brain Infarction - etiology
Disease Models, Animal
Drug Administration Schedule
Endothelium
Endothelium - drug effects
Enzymes
Fibrinolytic Agents - adverse effects
Granulocyte Colony-Stimulating Factor - administration & dosage
Hemorrhage
Hemorrhage - chemically induced
Infarction, Middle Cerebral Artery - drug therapy
Ischemia
Male
Matrix Metalloproteinase 9 - metabolism
Neutrophil Infiltration - drug effects
Neutrophils - drug effects
Neutrophils - metabolism
Peroxidase - metabolism
Rats
Rats, Inbred SHR
Reperfusion Injury - drug therapy
Reperfusion Injury - etiology
Rodents
Statistics, Nonparametric
Surgery
Time Factors
Tissue Plasminogen Activator - adverse effects
Veins & arteries
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Summary:Granulocyte colony-stimulating factor (G-CSF) is a pharmacologic agent inducing neutrophil mobilization and a new candidate for neuroprotection and neuroregeneration in stroke. Its effects when used in combination with tissue plasminogen activator (tPA) were explored during the acute phase of ischemic stroke. We used a middle cerebral artery occlusion (MCAO) model of cerebral ischemia, associated with treatment with tPA, in male spontaneously hypertensive rats (SHR). Granulocyte colony-stimulating factor (G-CSF; 60 μg/kg) was injected just before tPA. Neutrophil response in peripheral blood and in the infarct area was quantified in parallel to the infarct volume. Protease matrix metallopeptidase 9 (MMP-9) release from circulating neutrophils was analyzed by immunochemistry and zymography. Vascular reactivity and hemorrhagic volume in the infarct area was also assessed. Twenty four hours after ischemia and tPA, G-CSF administration induced a significant increase of neutrophils in peripheral blood (P
ISSN:1742-2094
1742-2094
DOI:10.1186/1742-2094-11-96