Introduction: Remote ischemic preconditioning (RIP) is a form of endogenous adaptive response that may be induced by periodic alternating of short cycles of ischemia and reperfusion in organs distant from the heart, thereby inducing effective cardioprotection against ischemic reperfusion (IR) injury. It is known from experimental studies that hearts with acute STZ-induced diabetes, except harmful effects, also exhibit partial adaptation to calcium overload, hypoxia and ischemia-reperfusion injury. However, the link between diabetes mellitus and remote preconditioning is not fully understood.
Objectives: To examine the impact of acute diabetes, remote preconditioning and their combination on IR injury in the isolated rat heart.
Materials and methods: We used 9-10 weeks old male Wistar rats in our experiments. They were kept on standard pellet diet in 12L/12D regimen at 22-23oC with free access to food and water. Acute diabetes mellitus was induced by a single dose of streptozotocin (STZ, 65 mg/kg, i.p.). Experiment was terminated on the 8-day after STZ application. At that time, diabetic animals exhibited significantly increased glucose, glycohemoglobin, cholesterol, triglycerides, as well as decreased insulin levels in blood. Diabetic and non-diabetic rats were subjected to remote preconditioning induced by 3 cycles of 5 minutes ischemia (occlusion of the femoral artery) / 5 min reperfusion in right hind limb. Subsequently, the hearts were perfused according to Langendorff technique using a protocol of global ischemia (30 min) and reperfusion (40 min). Cardiac functional parameters (HR, CF, LVSP, LVDiP, LVDP, +dP/dtmax, -dP/dtmax) were recorded during the protocol of IR.
Results: Baseline pre-ischemic parameters did not differ between the groups. We observed a significantly better post-ischemic restoration of systolic and diastolic function compared with non-adapted controls, in all three adapted groups. In addition, recovery of cardiac function did not differ between these groups indicating that application of RIP in the diabetic hearts did not result in further increase in their resistance against IR.
Conclusion: The results suggest that similar protective mechanisms as in the myocardium exposed to RIP are apparently involved in the mechanisms of reduced sensitivity of the diabetic hearts against IR.