EISSN: 2980-0749
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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

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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