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5-(N-Ethyl-N-isopropyl)-amiloride, an Na(+)-H(+) exchange inhibitor, protects gerbil hippocampal neurons from ischemic injury.

Abstract
The effect of the selective Na(+)/H(+) antiporter inhibitor 5-(N-ethyl-N-isopropyl)-amiloride (EIPA) on cerebral ischemia/reperfusion injury was evaluated in the Mongolian gerbil. Ischemia was induced in unanaesthetized gerbils by a 5-min period of bilateral common carotid artery occlusion followed by reperfusion for 6 days. Two groups of gerbils were injected intraperitoneally with either dimethyl sulfoxide (DMSO; 10 microl) or EIPA (5 mg/kg in 10 microl DMSO) 30 min prior to ischemia. The increase in locomotor activity in the EIPA-treated group was significantly less than that of the control group at both 24 h and 6-day post-ischemia. The extent of CA1 pyramidal neuron loss was significantly reduced in the EIPA-treated group in comparison with that of DMSO treated controls. These results suggest that EIPA can protect cerebral neurons from ischemia/reperfusion injury and implicates acidosis and Na(+)/H(+) exchange as a causative factor in such injury.
AuthorsJ W Phillis, A Y Estevez, L L Guyot, M H O'Regan
JournalBrain research (Brain Res) Vol. 839 Issue 1 Pg. 199-202 (Aug 21 1999) ISSN: 0006-8993 [Print] Netherlands
PMID10482815 (Publication Type: Journal Article)
Chemical References
  • Neuroprotective Agents
  • Sodium-Hydrogen Exchangers
  • Amiloride
  • ethylisopropylamiloride
Topics
  • Amiloride (analogs & derivatives, pharmacology)
  • Animals
  • Brain Ischemia (prevention & control)
  • Gerbillinae
  • Hippocampus (blood supply, drug effects, pathology)
  • Male
  • Neurons (drug effects)
  • Neuroprotective Agents (pharmacology)
  • Reperfusion Injury (prevention & control)
  • Sodium-Hydrogen Exchangers (antagonists & inhibitors)

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