İskemi-Reperfüzyon Hasarı

Abstract

Genel kanı olarak, reperfüzyon hasarı, epikardial büyüme ve antegrat kan akımının normale dönmesiyle ilişkili infarksiyon sürecinin bir bileşeni olmasına rağmen, kateterizasyon laboratuvarında, iskemi - reperfüzyon hasarı (İ/R) sık sık “no reflow” fenomeni ile eş anlamlı olarak kullanılır. Reperfüzyon sırasında ise, iyon akışında hızlı bir değişim meydana gelir ve pH’ın normale dönüşü sırasında sitotoksisite oluşur. Na⁺ - H⁺ ve Na⁺ - HCO3⁺ transportunu içeren Na⁺ bağımlı pH düzenleme mekanizmaları aktive olur ki bu olay hücre içi Na⁺ birikimine yol açar. Yüksek Na⁺ konsantrasyonu Na⁺ - Ca⁺ değişimi ile intraselüler Ca⁺ konsantrasyonunu artırır. Hücre içinde Ca⁺² iyon konsantrasyonunun artışı hücre için sitotoksiktir. Kardiyak cerrahi sonucu ortaya çıkan İ/R, spontan miyokart infarktüsüne bağlı olan İ/R’den farklıdır. Cerrahi tamamlandığında kros klemp kaldırılır, kalp birden bire yüksek oranda antikoagülan içeriği olan, kardiyopulmoner baypas cihazının immünolojik etkilerine maruz kalmış ve yüksek oranda oksijen içeren kan ile reperfüze olur. Sonuç olarak, kardiyak cerrahi sonrası myokard, aşırı iskemi ve reperfüzyona maruz kalır. Klinik olarak ameliyat sonrası İ/R hasarı; aritmi, myokardiyal stunning, düşük kalp debisi veya ameliyat sonrası miyokart infarktüsü ile kendini gösterebilir. Kardiyak cerrahide kalp korunmasında en önemli köşe taşı kardiyoplejik solüsyondur. Bu solüsyon potasyum, mannitol ve glukoz içerir. Arrest edilmiş ve soğutulmuş kalpte metabolik ihtiyaçlar minimize edilmiş olur. Yıllar içinde gelişen tecrübeyle birlikte, kardiyoplejik solüsyonların içeriklerinde ufak değişiklikler meydana gelmiştir. Tüm bunlara rağmen kardiyopleji sonrası İ/R hala gözlemlenmektedir.

Keywords

• Hasar,iskemi-reperfüzyon,açık kalp cerrahisi,miyokart

Ischemia-Reperfusion Injury

Abstract

While reperfusion injury is widely considered to represent a component of the infarction process related to epicardial growth and normalization of antegrade blood flow, the term ischemia/reperfusion (I/R) injury is frequently used synonymously with the “no reflow” phenomenon.  I/R injury after cardiac surgery is completely different from I/R injury after spontaneous myocardial infarction (MI). During reperfusion, ion transfer is rapidly altered and cytotoxicity develops as pH is normalized. Na⁺ dependent pH regulation mechanisms such as, Na⁺ - H⁺ and Na⁺ - HCO³⁺ transport are activated, triggering the accumulation of intracellular Na⁺. Elevated intracellular Na+ levels are associated with increased intracellular Ca⁺² concentrations through the activity of the Na⁺ - Ca⁺² exchanger. Elevated Ca⁺² ion concentrations have a cytotoxic impact. After completion of the surgical procedure, when the cross clamp is released, the cardiac tissues are re-perfused with a highly anticoagulated and oxygenated blood, which is affected from the immunological effects of the cardiopulmonary bypass pump. Thus, after cardiac surgery myocardium is exposed to excessive ischemia and reperfusion injury that may manifest themselves as arrhythmias, myocardial stunning, low cardiac output or postoperative MI. The cornerstone of the myocardial protection during cardiac surgery is the use of cardioplegic solutions containing potassium, mannitol and glucose. The metabolic requirements are minimized by myocardial arrest. Although the composition of cardioplegic solutions evolves with accumulating experience, I/R injury still occurs after cardioplegia.

Keywords

• Injury,ischemia-reperfusion,open heart surgery,myocardium

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