2020, Cilt 18, Sayı 3, Sayfa(lar) 115-120 |
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Nitric Oxide and C-Reactive Protein Levels in Ischemic Stroke |
Sibel Bilgili1, Gizem Yalçın1, Giray Bozkaya1, Nuriye Uzuncan1, Arife Erdoğan2 |
1Sağlık Bilimleri Üniversitesi İzmir Bozyaka Eğitim Ve Araştırma Hastanesi, Tıbbi Biyokimya, İzmir, Türkiye 2İzmir Çiğli Bölge Eğitim Hastanesi, Acil Tıp, İzmir, Türkiye |
Keywords: Nitric Oxide, C-Reactive Protein, ischemic Stroke |
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Purpose: Nitric oxide(NO) is one of the important substances that are synthesized to keep the blood
vessels dilated enough to provide adequate flow and to maintain cerebrovascular homeostasis. Creactive
protein(CRP) is a highly sensitive indicator of inflammation and tissue damage. High CRP
concentrations are thought to have effects such as dysfunction of vascular endothelium and decreased
NO release. The purpose of this study was to investigate the levels of CRP and NO and to see the
correlation of these markers in ischemic stroke patients.
Material and Methods: Fifty ischemic stroke patients and 31 healthy control group were included in
this study. Ischemic stroke was differentiated by computerized tomography scan. The patients blood
samples were taken at admission to the emergency department, within 24 hours of stroke symptom
onset, before any treatment was given. Serum CRP and NO levels were evaluated.
Results: The mean serum NO concentration of the patients (6.52±9.52 μmol/L) was significantly lower
than control group (20.48±22.17 μmol/L) (p<0.01). Serum CRP levels in patients (13.47±18.58 mg/L)
significantly higher than the control group (1.98±1.37 mg/L) (p<0.01). There was no significant
correlation between NO and CRP levels (p>0.05).
Conclusion: Although we found decreased NO levels and increased CRP levels in the patients, there
was no correlation between these two. The results of this study show NO’s possible role in
neuroprotection and increased levels of CRP may be associated with ischemic stroke. Further studies
are necessary to assess the functional interactions between CRP and NO and their contribution to the
pathophysiology of cerebral ischemia. |
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Abstract
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