Asfiksiyal Kardiyak Arrestli Rat Modelinde Böbrek Histopatolojisi ve Tümör Nekrozis Faktör-α Ekspresyonu

Kardiyak arrest (KA) sonrası post-kardiyak arrest sendromu (PKAS) olan hastalarda çoklu organ hasarı mortalite ile ilişkilidir. Spontan dolaşıma dönüş (SDD) sonrası çoklu organ hasarları arasında böbrek fonksiyon bozukluğu, yüksek mortalite ile ilişkili olduğu bilinen akut böbrek hasarına yol açabilir. Bu böbrek hasarı, KA’yı takiben SDD tarafından iskemi-reperfüzyonun aracılık ettiği sistemik bir infl amatuar yanıt sendromu ile ilişkilidir. Ancak, bunun mekanizması belirsizliğini korumaktadır. Bu nedenle, bu çalışmanın amacı, bir proinfl amatuar sitokin olan tümör nekrozis faktör-α (TNF-α) ekspresyonu ile PKAS’ta böbrek hasarı arasındaki ilişkiyi belirlemekti. Çalışmada, normotermik Sprague-Dawley ratlarda asfiksiyal KA indüklendi ve ratların hayatta kalma oranı SDD’den iki gün sonra ölçüldü. Her gruptan ratlar (n=6), SDD’den 6 saat, 12 saat, 1 gün ve 2 gün sonra sakrifiye edildi. Böbrek hasarı Masson trikrom boyama, TNF-α immünohistokimyasal (IHC) yöntem ve western blot ile analiz edildi. SDD’den 12 saat sonra mortalite %72 iken, SDD’den 2 gün sonra ratlarda hayatta kalma oranı %24’e düştü. KA sonrası böbrek dokusundaki histopatolojik skor, kontrol grubuna göre 6. saatte anlamlı bir artış gösterdi. Renal korteks dokusundaki TNF-α ekspresyon seviyesi, hem IHC hem de western blot analiz sonuçlarına göre KA’dan 6 saat sonra arttı. KA’dan sonra, böbrek histopatolojik hasarı, böbrek dokusunda orantılı bir TNF-α ekspresyon artışı ile birlikte böbrekte hızlı hasara yol açan SDD’den 6 saat sonra önemli ölçüde arttı.

Histopathology and Tumor Necrosis Factor-α Expression in The Kidney of an Asphyxial Cardiac Arrest Rat Model

Multiple organ injuries in patients with post cardiac arrest syndrome (PCAS) after cardiac arrest (CA) is associated with mortality. Among multiple organ injuries after return of spontaneous circulation (ROSC), renal dysfunction can lead to acute kidney injury, which is known to be associated with high mortality. This renal injury is associated with a systemic infl ammatory response syndrome mediated by ischemia reperfusion by ROSC following CA. However, the mechanism remains unclear. Therefore, the objective of this study was to determine, the relationship between the expression of tumor necrosis factor-α (TNF-α), a pro-infl ammatory cytokine, and renal injury in PCAS. In the present study, asphyxial CA was induced in Sprague-Dawley rats with normothermia and the survival rate was measured at two days after ROSC. The rats in each group (n=6) were sacrificed at 6 h, 12 h, 1 day, and 2 days after ROSC. Renal injury was analyzed with by Masson’s trichrome stain, TNF-α immunohistochemistry (IHC) and western blot. The mortality was 72% at 12 h after ROSC and the survival rate of rats was decreased to 24% 2 days after ROSC. Histopathological score in the renal tissue after CA showed a significant increase at 6 h than sham group. The expression level of TNF-α in the renal cortex tissue was also increased at 6 h after CA based on both IHC and western blot results. After CA, the renal histopathological injury was significantly increased at 6 h after ROSC with a proportional increase of TNF-α expression in the kidney tissue leading to rapid injury to the kidney.

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Kafkas Üniversitesi Veteriner Fakültesi Dergisi-Cover
  • ISSN: 1300-6045
  • Yayın Aralığı: Yılda 6 Sayı
  • Başlangıç: 1995
  • Yayıncı: Kafkas Üniv. Veteriner Fak.
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