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Nitric Oxide Measured by a Porphyrinic Micro Sensor in Rat Brain after Transient Middle Cerebral Artery Occlusion

Journal of Cerebral Blood Flow & Metabolism · 1993 · Vol. 13(3) · pp. 355–358
T. MalinskiFreddie BaileyZ. G. ZhangMichael Chopp

Abstract

We measured, in vivo, the local concentration of nitric oxide (NO) in cerebral tissue, during and after transient middle cerebral artery occlusion in the rat (n = 8). Baseline concentration of NO was < 10(-8) M; upon initiation of ischemia, NO concentration increased to approximately 10(-6) M and then declined. Reperfusion likewise stimulated an increase in NO concentration to above baseline level. Administration of N-nitro-L-arginine methyl ester (n = 4), an inhibitor of nitric oxide synthase, before onset of ischemia, maintained NO at basal levels. Our data indicate that large increases in NO occur at onset of ischemia, which may affect tissue response to an ischemic insult.

Nitric Oxide and Endothelin EffectsAnalytical Chemistry and SensorsMolecular Sensors and Ion DetectionNitric oxideIschemiaMiddle cerebral arteryNitric oxide synthaseOcclusionIn vivoAnesthesiaInternal medicineMedicineChemistry

MeSH terms

AnimalsArginineBrainIschemic Attack, TransientMaleMetalloporphyrinsNitric OxideOsmolar ConcentrationReperfusionRats, WistarNG-Nitroarginine Methyl EsterRats
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