Induction of nitric oxide synthase activity in rodent brain following middle cerebral artery occlusion

Induction of nitric oxide synthase activity in rodent brain following middle cerebral artery... The conversion of l -( 3 H)arginine to l -( 3 H)citrulline in the absence of calcium can be used to assay selectively the activity of inducible nitric oxide synthase (NOS) in rat spleen homogenates 6 h after lipopolysaccharide administration. Using similar assay conditions, changes in inducible NOS activity were measured within ischemic brain tissue between 2 h and 7 days following permanent middle cerebral artery (MCA) occlusion in Sprague-Dawley rats and SV-129 mice. Total (constitutive and inducible) NOS activity was measured in the presence of 0.5 mM CaCl 2 . Whereas total NOS activity in rat decreased dramatically to 16% and 6% of baseline 6 and 12 h after MCA occlusion, inducible NOS activity remained undetectable before 2 days after occlusion, became maximal at 3 days, and decreased to less than 10% of maximal iNOS activity at 7 days. In the mouse, total NOS activity decreased after MCA occlusion but inducible NOS activity was undetectable from 2 h to 4 days after occlusion. Sustained NO production by inducible NOS activity does not contribute to ischemic injury within 24 h after MCA occlusion, but may contribute to infarct maturation 2–4 days after ischemia in some but not all species. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neuroscience Letters Elsevier

Induction of nitric oxide synthase activity in rodent brain following middle cerebral artery occlusion

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Abstract

The conversion of l -( 3 H)arginine to l -( 3 H)citrulline in the absence of calcium can be used to assay selectively the activity of inducible nitric oxide synthase (NOS) in rat spleen homogenates 6 h after lipopolysaccharide administration. Using similar assay conditions, changes in inducible NOS activity were measured within ischemic brain tissue between 2 h and 7 days following permanent middle cerebral artery (MCA) occlusion in Sprague-Dawley rats and SV-129 mice. Total (constitutive and inducible) NOS activity was measured in the presence of 0.5 mM CaCl 2 . Whereas total NOS activity in rat decreased dramatically to 16% and 6% of baseline 6 and 12 h after MCA occlusion, inducible NOS activity remained undetectable before 2 days after occlusion, became maximal at 3 days, and decreased to less than 10% of maximal iNOS activity at 7 days. In the mouse, total NOS activity decreased after MCA occlusion but inducible NOS activity was undetectable from 2 h to 4 days after occlusion. Sustained NO production by inducible NOS activity does not contribute to ischemic injury within 24 h after MCA occlusion, but may contribute to infarct maturation 2–4 days after ischemia in some but not all species.

Journal

Neuroscience LettersElsevier

Published: Jul 21, 1995

References

  • The complex role of nitric oxide in the pathophysiology of focal cerebral ischemia
    Dalkara, T.; Moskowitz, M.A.
  • l -Arginine decreases infarct size caused by middle cerebral artery occlusion in SHR
    Morikawa, E.; Huang, Z.; Moskowitz, M.A.
  • Evidence for an astrocyte-derived vasorelaxing factor with properties similar to nitric oxide
    Murphy, S.; Minor, R.L.; Welk, G.; Harrison, D.G.
  • Studies on functional and metabolic role of urea cycle intermediates in brain
    Sadasivudu, B.; Rao, T.I.

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