Cardioprotective effect of postconditioning against ischemia-reperfusion injury is lost in heart of 8-week diabetic rat


Altunkaynak H. O., ÖZÇELİKAY A. T.

GENERAL PHYSIOLOGY AND BIOPHYSICS, cilt.35, sa.1, ss.63-69, 2016 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 35 Sayı: 1
  • Basım Tarihi: 2016
  • Doi Numarası: 10.4149/gpb_2015032
  • Dergi Adı: GENERAL PHYSIOLOGY AND BIOPHYSICS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.63-69
  • Anahtar Kelimeler: Ischemia, Reperfusion, Heart, Postconditioning, Rat, ACUTE MYOCARDIAL-INFARCTION, SHORT-TERM, TOLERANCE, INSULIN, INVOLVEMENT, MECHANISMS, MORTALITY, MELLITUS, MODELS, TYPE-2
  • Ankara Üniversitesi Adresli: Evet

Özet

Although ischemic preconditioning (IPC) and ischemic postconditioning (IPost) result in protection against ischemia-reperfusion (I/R) injury in healthy hearts, pathological conditions such as diabetes can modify the protective effects of IPC and IPost. There are a few studies concerning the effect of IPost only in diabetic hearts which have similar or decreased tolerance to I/R injury. In the present study we investigated the effects of IPost in diabetic hearts which had increased tolerance to I/R injury. Isolated hearts from control and diabetic rats were subjected to global ischemia (40 min) followed by reperfusion (40 min). IPost was induced by six cycles (10 s) of reperfusion and ischemia after the global ischemia. After I/R, cardiac recovery in diabetic hearts was better than that in control hearts. IPost did not produce any further protection in the diabetic hearts whereas it resulted in a significant recovery in the control hearts. Similarly, the decreased troponin I (TnI) levels of diabetic hearts did not change after IPost. However, IPost significantly lowered the increase in TnI levels of control hearts. In conclusion, these results show that IPost can not produce a further protection in the hearts of 8 -week diabetic rats which have increased tolerance to I/R injury.