Preservation of N-Methyl-D-Aspartate (NMDA)-induced cerebral arteriolar dilation after ischemia by a protein synthesis inhibator

D. W. Busija, F. Domoki, R. Veltkamp, F. Bari, T. M. Louis

Research output: Contribution to journalArticle

Abstract

Cerebral arteriolar dilation to NMDA is reduced by global ischemia. We tested the hypothesis that pretreatment with an inhibitor of protein synthesis would preserve NMDA-induced arteriolar dilation after ischemia. Pial arteriolar diameters were measured in piglets using a closed cranial window and intravital microscopy. Baseline arteriolar diameters were approximately 100 μm. Total, global ischemia was induced by increasing intracranial pressure for 10 minutes. Prior to ischemia, NMDA dilated pial arterioles by 10±2% at 10-5M and 37±7% at 10-4 M (mean ±sem; n=5). At one hour after ischemia, 10-5M failed to dilate arterioles and arteriolar dilation to 10-4M was reduced to 16±5% (p-5M and 35±6% at 10-4M (n=5; p>0.05). Similarly, arteriolar dilation to NMDA was intact at 2 and 4 hours. We conclude that inhibition of protein synthesis preserves normal arteriolar dilation to NMDA after ischemia.

Original languageEnglish
JournalFASEB Journal
Volume12
Issue number5
Publication statusPublished - Mar 20 1998

Fingerprint

N-Methylaspartate
aspartic acid
ischemia
Dilatation
Ischemia
protein synthesis
Proteins
Arterioles
preserves
Protein Synthesis Inhibitors
protein synthesis inhibitors
Intracranial Pressure
piglets
microscopy
pretreatment

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Preservation of N-Methyl-D-Aspartate (NMDA)-induced cerebral arteriolar dilation after ischemia by a protein synthesis inhibator. / Busija, D. W.; Domoki, F.; Veltkamp, R.; Bari, F.; Louis, T. M.

In: FASEB Journal, Vol. 12, No. 5, 20.03.1998.

Research output: Contribution to journalArticle

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AU - Louis, T. M.

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N2 - Cerebral arteriolar dilation to NMDA is reduced by global ischemia. We tested the hypothesis that pretreatment with an inhibitor of protein synthesis would preserve NMDA-induced arteriolar dilation after ischemia. Pial arteriolar diameters were measured in piglets using a closed cranial window and intravital microscopy. Baseline arteriolar diameters were approximately 100 μm. Total, global ischemia was induced by increasing intracranial pressure for 10 minutes. Prior to ischemia, NMDA dilated pial arterioles by 10±2% at 10-5M and 37±7% at 10-4 M (mean ±sem; n=5). At one hour after ischemia, 10-5M failed to dilate arterioles and arteriolar dilation to 10-4M was reduced to 16±5% (p-5M and 35±6% at 10-4M (n=5; p>0.05). Similarly, arteriolar dilation to NMDA was intact at 2 and 4 hours. We conclude that inhibition of protein synthesis preserves normal arteriolar dilation to NMDA after ischemia.

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