Dual effects of L-NAME during transient focal cerebral ischemia in spontaneously hypertensive rats

The role of nitric oxide (NO) in ischemic neuronal injury is unclear. In permanent focal ischemia models, NO release has been reported to be both neuroprotective, by virtue of actions to improve cerebral blood flow (CBF) within ischemic tissue, and neurotoxic. Very little attention has been given to determining the role of NO in transient focal ischemia. In the present studies, low-dose NO inhibition using NG-nitro-L-arginine methyl ester (L-NAME; 0.1 mg/kg bolus, 0.01 mg.kg-1.min-1 iv) reduced infarct volume after 180 min of middle cerebral arterial occlusion (MCAO) and 120 min of reperfusion as measured via 2,3,5-triphenyltetrazolium chloride by 55% (P