Objective Study on the effect of diabetes on protection of ischaemia Postconditioning in myocardial ischaemia-reperfusion injury in isolated rat hearts.

Methods The type 2 diabetic rats were induced by the intravenous injection of streptozotocin (STZ) and high caloric diet. 60 Wister rats were divided into three groups randomly. Ischaemia- reperfusion in nomal rats (A group), ischaemia postconditioning in nomal rats (B group), ischaemia postconditioning in diabetic rats (C group). Rats were used for Langendorff isolated heart perfusion with 30 min of globe ischaemia and 60 min of reperfusion, then the models of Ischaemia- reperfusion (A) were made. But to B and C, rat hearts were subjected to six cycles of 10 s of globe ischaemia and 10 s of reperfusion as ischaemia postconditioning during the early minutes of reperfusion. The levels of lactate dehydrogenase (LDH) in the coronary effluent and infarction size was determined by TTC staining. Phosphorylation of akt and gsk-3β were analysed by western blotting and immunohistochemical staining.

Results Ischemic postconditioning reduced LDH, CK and improved the haemodynamic parameters and reduced myocardial infarction size (29.50±3.4% vs 45.65±4.8%), phospho-Akt and phospho-GSK-3β expression increased markedly in B group. But compared A group there were no parently diffrence in C group. The level of LDH, CK didn't decline and the myocardial infarction size were not reduced. phospho-Akt and phospho-GSK-3β expression in C group is more less than in B group.

Conclusion Ischemic postconditioning may significantly protect myocardium from reperfusion injury in isolated normal rat hearts. But in diabetic rats, the protection of Ischaemic postconditioning has no effect, the mechanism of this phenomenon maybe connected with lower expression of Phosphorylation of Akt and GSK-3β in the condition of diabetic and impaired Reperfusion Injury Salvage Kinase (RISK) signalling pathway (RISK pathway).