Authors: R Taffi L Nanetti L Mazzanti M Bartolini A Vignini F Raffaelli P Pasqualetti F Vernieri L Provinciali M Silvestrini
Publish Date: 2007/12/19
Volume: 255, Issue: 1, Pages: 94-98
Abstract
Production of reactive oxygen species after cerebral blood flow disruption may enhance tissue damage through multiple molecular pathways Changes in nitric oxide NO metabolism and oxidative stress status were investigated in 47 patients with ischemic stroke by measuring plasma nitric oxide NO and peroxynitrite ONOO– levelsA correlation was sought between these two parameters and i baseline stroke severity based on the National Institute of Health stroke scale NIHSS and ii neurological outcome in terms of NIHSS changes from entry T0 to 30 days after symptom onset T1 The control group consisted of 30 age and sexmatched healthy subjects Mean plasma levels of ONOO– arbitrary fluorescence number ± SD were significantly higher in patients 770 ± 171 vs 535 ± 069 p 0001 whereas mean NO levels nmol/mg protein were significantly higher in controls 11540 ± 1240 vs 5110 ± 1250 p 0001 Plasma ONOO– was significantly higher among patients with nonlacunar stroke 848 ± 150 vs 695 ± 158 in those with lacunar stroke p = 0001 whereas NO levels were significantly higher among lacunar stroke patients 6000 ± 786 vs 4177 ± 929 in patients with nonlacunar stroke p 0001 Nitric oxide plasma levels were also associated with an unfavorable evolution in nonlacunar stroke since a 10 unit increase in NO predicted a 1 point reduction in the NIHSS score at T1 Findings show that changes in NO metabolism may be considered as markers of brain injury in patients with ischemic stroke Further work is needed to establish whether the amount of biochemical changes related to oxidative stress may influence outcome in these patients
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