İskemi-Reperfüzyon Hasarı

Year 2015, Volume: 18 Issue: 2, 89 - 93, 03.08.2015

Çetin Murat Songur

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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