Polymorphonuclear neutrophils contribute to infarction and oxidative stress in the cortex but not in the striatum after ischemia-reperfusion in rats

Brain Res. 2003 Oct 10;987(1):32-8. doi: 10.1016/s0006-8993(03)03224-4.


The present work examined whether polymorphonuclear neutrophil (PMN) infiltration contributes to cortical and striatal brain damage and oxidative stress in a model of transient focal cerebral ischemia. A 2-h occlusion of the left middle cerebral artery and ipsilateral common carotid artery was performed in rats. Administration of the neutropenic agent vinblastine (0.5 mg/kg, i.v.) resulted in a profound decrease in circulating PMNs which was associated with a 80% decrease in myeloperoxidase activity, a marker of PMN infiltration, in both the cortex and the striatum. In the cortex, vinblastine-treated animals exhibited a 44% decrease in the infarct volume and also reduced the oxidative stress (evaluated by the decrease in glutathione concentrations). By contrast, in the striatum, neutropenia modified neither the lesion size nor the oxidative stress. These results indicate that PMN contribution to postischemic injury and oxidative stress is dependent on the brain structure.

MeSH terms

  • Animals
  • Antineoplastic Agents, Phytogenic / pharmacology
  • Brain Ischemia / drug therapy
  • Brain Ischemia / enzymology
  • Brain Ischemia / metabolism*
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / enzymology
  • Cerebral Cortex / metabolism*
  • Corpus Striatum / metabolism
  • Male
  • Neutrophil Infiltration*
  • Neutrophils / metabolism*
  • Oxidative Stress*
  • Peroxidase / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / drug therapy
  • Reperfusion Injury / enzymology
  • Reperfusion Injury / metabolism*
  • Vinblastine / pharmacology


  • Antineoplastic Agents, Phytogenic
  • Vinblastine
  • Peroxidase