Chapter

Brain Edema XIII

Volume 96 of the series Acta Neurochirurgica Supplementum pp 263-266

Increased substance P immunoreactivity and edema formation following reversible ischemic stroke

  • R. J. TurnerAffiliated withDepartment of Pathology, University of Adelaide
  • , P. C. BlumbergsAffiliated withDepartment of Pathology, University of AdelaideCentre for Neurological Diseases, Hanson Institute
  • , N. R. SimsAffiliated withDepartment of Medical Biochemistry and Centre for Neuroscience, School of Medicine, Flinders University
  • , S. C. HelpsAffiliated withDepartment of Medical Biochemistry and Centre for Neuroscience, School of Medicine, Flinders University
  • , K. M. RodgersAffiliated withDepartment of Pathology, University of Adelaide
  • , R. VinkAffiliated withDepartment of Pathology, University of Adelaide

Summary

Previous results from our laboratory have shown that neurogenic inflammation is associated with edema formation after traumatic brain injury (TBI). This neurogenic inflammation was characterized by increased substance P (SP) immunoreactivity and could be attenuated with administration of SP antagonists with a resultant decrease in edema formation. Few studies have examined whether neurogenic inflammation, as identified by increased SP immunoreactivity, occurs after stroke and its potential role in edema formation. The present study examines SP immunoreactivity and edema formation following stroke.

Experimental stroke was induced in halothane anaesthetized male Sprague-Dawley rats using a reversible thread model of middle cerebral artery occlusion. Increased SP immunoreactivity at 24 hours relative to the non-infarcted hemisphere was observed in perivascular, neuronal, and glial tissue, and within the penumbra of the infarcted hemisphere. It was not as apparent in the infarct core. This increased SP immunoreactivity was associated with edema formation. We conclude that neurogenic inflammation, as reflected by increased SP immunoreactivity, occurs following experimental stroke, and that this may be associated with edema formation. As such, inhibition of neurogenic inflammation may represent a novel therapeutic target for the treatment of edema following reversible, ischemic stroke.

Keywords

Ischemia edema neuropeptides inflammation