Nitric oxide (NO) is involved in the autoregulation of cerebral blood flow and in modulation of the
respiratory chain activity in the normal brain. The present study aimed to evaluate the role of NO under
two levels of partial brain ischemia induced by unilateral or bilateral carotid artery occlusion
(UCO/BCO), for 24 hours and in appropriate control groups.
Time-sharing fluorometer/reflectometer was used for the monitoring of mitochondrial NADH, by the
fluorometric technique and oxyhemoglobin level by 2 wavelength reflectance method, combined with
laser Doppler flowmetry for cerebral blood flow (CBF) monitoring. Systemic blood pressure (MAP)
was also monitored. L-NAME was used for the inhibition of NO synthesis while nitrite was used as an
exogenous source for NO. In both groups of ischemic animals L-NAME induced an increase in MAP
and oxigenation of HbO2 however in the UCO group CBF remained stable and NADH was oxidized
whereas in the BCO group CBF decreased with no change in NADH. Following nitrite infusion MAP
reversibly decreased, CBF increased, HbO2 and NADH remained low in the BCO group with a slight
reversible increase of NADH in the UCO group.
In conclusion, it seems that NO plays an important role in the autoregulation of CBF and mitochondrial
activity in the partially ischemic brain.
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