Effects of L‐arginine on the brain ischaemia‐reperfusion damage in rats: An investigation by somatosensory evoked potentials and histopathology

Abstract

We investigated whether administration of L‐arginine reduces the ischaemia‐reperfusion damage in the rat brain. The effects of L‐arginine were evaluated by means of somatosensory evoked potential (SEP) measurements and quantitative histopathological investigations. There was no significant difference between groups based on SEP data. The results obtained from quantitative histopathological investigations indicate that the nitric oxide (NO) precursor L‐arginine does not appear to have a protective effect on the brain ischaemia‐reperfusion damage. Furthermore, histopathological evaluation revealed a higher number of damaged cells in the L‐arginine treated rats than in control group. The results of the present study suggest that high concentrations of L‐arginine present in later stages of reperfusion might have harmful effects on reperfusion damage in the brain.

Nitric Oxide-Dependent Pathways as Critical Factors in the Consequences and Recovery after Brain Ischemic Hypoxia

“…The administration of L-arginine increased regional blood flow and prevented tissue damage in the rat MCAO model [135][136][137]. However, contradictory results with L-arginine administration were obtained that showed a beneficial effect [135][136][137], no effect [138] and the potentiation of pathological changes [139,140]. These effects may result from the fact that L-arginine enhances NO • synthesis via all three isoforms [141]; therefore, synthesis of potentially detrimental NO • from iNOS or nNOS may counteract the neuroprotective effects of eNOS activation.…”