Altunkaynak Hande O, Ozcelikay Arif T
Department of Pharmacology, Faculty of Medicine, Baskent University, Ankara, Turkey.
Gen Physiol Biophys. 2016 Jan;35(1):63-9. doi: 10.4149/gpb_2015032. Epub 2015 Oct 22.
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.
尽管缺血预处理(IPC)和缺血后处理(IPost)可对健康心脏的缺血再灌注(I/R)损伤起到保护作用,但诸如糖尿病等病理状况会改变IPC和IPost的保护效果。仅有少数研究关注了IPost对糖尿病心脏的影响,这些糖尿病心脏对I/R损伤的耐受性相似或降低。在本研究中,我们调查了IPost对I/R损伤耐受性增强的糖尿病心脏的影响。将来自对照大鼠和糖尿病大鼠的离体心脏进行整体缺血(40分钟),随后再灌注(40分钟)。整体缺血后,通过6个周期(每个周期10秒)的再灌注和缺血诱导IPost。I/R后,糖尿病心脏的心脏功能恢复优于对照心脏。IPost对糖尿病心脏未产生进一步的保护作用,而对对照心脏则导致了显著的恢复。同样,糖尿病心脏中降低的肌钙蛋白I(TnI)水平在IPost后未发生变化。然而,IPost显著降低了对照心脏中TnI水平的升高。总之,这些结果表明,IPost对I/R损伤耐受性增强的8周龄糖尿病大鼠心脏不能产生进一步的保护作用。