Mehmet Sinan DAL, Recep DEMİRBAĞ, Nurten AKSOY, Yusuf SEZEN, Mehmet UÇAR, Hakan BÜYÜKHATİPOĞLU, Timuçin AYDOĞAN, Mehmet Ali EREN, Turgay ULAŞ

Akut dekompanse kalp yetersizliği tedavisinin oksidatif stres üzerine etkisi

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

The effect of acute decompansated hearth failure treatment on oxidative stress

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

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