The effect of acute decompansated hearth failure treatment on oxidative stress

Results: We found CAT enzyme activities of patients with pre- and post-treatment groups were significantly lower than in control subjects (15.76±2.28 U/L; 17.36±1.55 U/L; 20.50±2.52 U/L, respectively, p

📌 3 Key Takeaways

🎯

Objective & Hypothesis:Objectives: Myocardial dysfunction in patients with hearth failure is suggested to occur due to membrane changes caused by oxidative stress.

📊

Key Findings & Data:Materials and methods: We measured enzyme activities of catalase (CAT) and lipid hydroperoxide (LOOH) from blood samples of 67 patients with decompensate hearth failure (pre-treatment group), who have compensated with the treatment (post-treatment group, n=54) according to clinical findings and two-dimensional echocardiography and 47 healthy volunteers (control group).

💡

Conclusion & Impact:Results: We found CAT enzyme activities of patients with pre- and post-treatment groups were significantly lower than in control subjects (15.76±2.28 U/L; 17.36±1.55 U/L; 20.50±2.52 U/L, respectively, p

🔬Design:Research Article

📍Scope:Comprehensive Sample

⚙️Variables:Domain Parameters

Abstract

Objectives: Myocardial dysfunction in patients with hearth failure is suggested to occur due to membrane changes caused by oxidative stress. The aim of this study is to evaluate whether there is a relationship between the degree of hearth failure and oxidative stress, and the effect of hearth failure therapy on oxidative stress parameters. Materials and methods: We measured enzyme activities of catalase (CAT) and lipid hydroperoxide (LOOH) from blood samples of 67 patients with decompensate hearth failure (pre-treatment group), who have compensated with the treatment (post-treatment group, n=54) according to clinical findings and two-dimensional echocardiography and 47 healthy volunteers (control group). Results: We found CAT enzyme activities of patients with pre- and post-treatment groups were significantly lower than in control subjects (15.76±2.28 U/L; 17.36±1.55 U/L; 20.50±2.52 U/L, respectively, p

Özet

Amaç: Kalp yetersizliği olan hastalarda miyokard disfonksiyonun, artmış oksidatif strese bağlı membran değişikliklerinden kaynaklanabileceği ileri sürülmektedir. Bu çalışmanın amacı oksidatif stres ile kalp yetersizliğindeki bozulmanın derecesi arasında bir ilişki olup olmadığını ve kalp yetersizliği tedavisinin oksidatif stres parametreleri üzerine etkisini araştırmaktır. Gereç ve yöntem: Klinik bulguları ve iki yönlü ekokardiyografi ile dekompanse kalp yetersizliği tanısı konulan 67 hasta (tedavi öncesi grup), tedavi ile kompansasyon sağlananlar (tedavi sonrası grup, n=54) ve 47 sağlıklı bireyden (kontrol grubu) alınan kan örneklerinden antioksidan enzimlerden katalaz (CAT) ve oksidan enzim olan lipit hidroperoksit (LOOH) aktiviteleri ölçüldü. Bulgular: CAT aktivitesi tedavi öncesi ve sonrası grupta kontrol grubuna göre istatistiksel olarak anlamlı düşük bulundu (sırasıyla 15.76±2.28 U/L; 17.36±1.55 U/L; 20.50±2.52 U/L, p

🔖

Cite This Article

DAL, M. S., DEMİRBAĞ, R., AKSOY, N., SEZEN, Y., UÇAR, M., BÜYÜKHATİPOĞLU, H., AYDOĞAN, T., EREN, M. A., ULAŞ, T. (2022). The effect of acute decompansated hearth failure treatment on oxidative stress. Journal of Clinical and Experimental Investigations, Cilt: 2 - Sayı: 3, 267–272. https://ajindex.com/articles/562027

📄 Full Text PDF Viewer

Open in New Tab ↗

↗New Tab

📄

PDF görüntüleyici hazırlanıyor...

References (14)

Singh A, Blackwell J, Neher J. Clinical inquiries. Does furosemide decrease morbidity or mortality for patients with diastolic or systolic dysfunction? J Fam Pract 2005; 54(4): 370-2
Despas F, Trouillet C, Franchitto N, et al. Levosimedan improves hemodynamics functions without sympathetic activation in severe heart failure patients: direct evidence from sympathetic neural recording. Acute Card Care 2010; 12(1): 25-30
Yeum KJ, Russell RM, Krinsky NI, Aldini G. Biomarkers of antioxidant capacity in the hydrophilic and lipophilic compartments of human plasma. Arch Biochem Biophys. 2004; 430(1): 97-103
Asiltürk Z, Nazlıgül Y, Yıldız M, Küçükazman M, Bulur O, Tezer A, et al. [Serum oxidative stress status in CagA positive Helicobacter pylori infection.] Klinik ve Deneysel Araştırmalar Dergisi 2011;2 (2); 202-6
McCormick ML, Denning GM, Reszka KJ, et al. Biological effects of menadione photochemistry: effects of menadione on biological systems may not involve classical oxidant production. Biochem J 2000; 350 Pt 3: 797-804
Carmody RJ, McGowan AJ, Cotter TG. Reactive oxygen species as mediators of photoreceptor apoptosis in vitro. Exp Cell Res 1999; 248(2): 520-30
Góth L. A simple method for determination of serum catalase activity and revision of reference range. Clin Chim Acta 1991; 196(2-3): 143-51
Arab K, Steghens JP. Plasma lipid hydroperoxides measurement by an automated xylenol orange method. Anal Biochem. 2004; 325(1): 158-63
Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989; 2(5): 358-67
Schiller NB, Acquatella H, Ports TA, et al. Left ventricular volume from paired biplane two-dimensional echocardiography. Circulation 1979; 60(3): 547-55
Hill MF, Singal PK. Antioxidant and oxidative stress changes during heart failure subsequent to myocardial infarction in rats. Am J Pathol 1996; 148(1): 291-300
Khaper N, Singal PK. Effects of afterload-reducing drugs on pathogenesis of antioxidant changes and congestive heart failure in rats. J Am Coll Cardiol 1997; 29(4): 856-61
Lucchesi BR. Modulation of leukocyte-mediated myocardial reperfusion injury. Annu Rev Physiol 1990; 52: 561-76
Ku DD. Coronary vascular reactivity after acute myocar