Abstract

Objective This study describes the protective effect of myocardial isehemic post- conditioning on ischemic-reperfused myocardium (I/ R) of diabetic rat and its Signaling mechanism. Methods Healthy SD rats weighing 25O-30Og were divided into 6 groups; (1) Blank control; (2) Ischemia-reperfusion; (3) Post conditioning; (4) Diabetic postconditioning ; (5) Diabetic ischemia-reperfusion; ( 6) Diabetic blank control group. Ten rats in each group were randomly selected. Introduction of diabetic rat model: 65 mg/kg STZ was injected into the intraperitoneal cavity, until 2 consecutive blood glucose measurements≥ 16.65 mmol/L were reached after48h. The diabetic model was successful when rats had following symptoms, such as more drinking, more eating, polyuria, weight loss and epilation. Langendorff isolated rat heart perfusion was used for the experiment. Following parameters were measured and compared: Coronary perfusion flow, myocardial infarct size, western blot for measurement of P-Akt, changes in myocardium and mitochondrian observed by Electron microscopy. Results Blood glucose concentration in diabetic group was (23. 15±2. 16) mmol/L and (4. 16±0. 31) mmol/L in non-diabetic group. There was a significant difference (P <0. 01) between the two groups. There were more coronary flow in post-conditioning groups (Post group and Dpost group) than ischemia-reperfusion groups (IR group and DIR group) (6.5±1.2、5.6±1.0 vs. 3.4±1.0、2.0±1.3). The myocardial infarction size was smaller in post-conditioning groups than in ischemia-reperfusion groups (25.2±2.1、34.2±3.6 vs. 47.5±3.5 、65.2±4.5). There was more expression of P-Akt and the myocardial fibers and mitochondrian in post-conditioning groups were better preserved. Conclusion Postconditioning has protective effects in diabetic rat hearts. The mechanism may be associated with Akt activation. Key words: Myocardial ischemia; Myocardial reperfusion injury; Diabetes mellitus P-Akt Postconditioning

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