Nitric oxide deficiency contributes to large cerebral infarct size

G. A. Kidd, L. W. Dobrucki, V. Brovkovych, David F. Bohr, T. Malinski

Research output: Contribution to journalArticle


The purpose of this study was to examine the role played by a deficit in nitric oxide (NO) in contributing to the large cerebral infarcts seen in hypertension. Cerebral infarction was produced in rats by occlusion of the middle cerebral artery (MCA). Studies were performed in Sprague-Dawley (SD) rats subjected to NO synthase blockade (N(G)-nitro-L-arginine [L-NNA], 20 mg · kg-1 · d-1 in drinking water) and in spontaneously hypertensive stroke-prone rats (SHRSP). NO released in the brain in response to MCA occlusion was monitored with a porphyrinic microsensor in Wistar-Kyoto rats. The increment in NO released with MCA occlusion was 1.31±0.05 μmol/L in L- NNA-treated rats, 1.25±0.04 μmol/L in SHRSP, 2.24±0.07 μmol/L in control SD rats, and 2.25±0.06 μmol/L in Wistar-Kyoto rats (P<0.0001 for control versus the other groups). Infarct sizes in the L-NNA-treated and control SD rats were 8.50±0.8% and 5.22±0.7% of the brain weights, respectively (P<0.05). The basilar arterial wall was significantly thicker in L-NNA- treated rats compared with their controls. We conclude that both the deficit in NO and the greater wall thickness contribute to the larger infarct size resulting from MCA occlusion in SHRSP and in L-NNA-treated rats compared with their respective controls.

Original languageEnglish (US)
Pages (from-to)1111-1118
Number of pages8
Issue number5
StatePublished - May 2000


  • Hypertension, NOS-deficiency
  • Infarct
  • Infarct size
  • Nitric oxide
  • Nitric oxide synthase
  • Stroke

ASJC Scopus subject areas

  • Internal Medicine

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