Changes in mitochondrial properties may contribute to enhanced resistance to ischemia–reperfusion injury in the diabetic rat heart

Abstract

Diabetes mellitus, besides having deleterious effects, induces cardiac adaptation that may reduce the heart's susceptibility to ischemia-reperfusion (IR) injury. This study aimed to investigate whether changes in mitochondrial properties are involved in the mechanisms of increased resistance of the diabetic heart to IR. Adult male Wistar rats were made diabetic by a single dose of streptozotocin (65 mg·kg, i.p.), and on the day 8, Langendorff-perfused hearts were subjected to 30 min global ischemia and 40 min reperfusion. Baseline preischemic parameters in the diabetic hearts did not differ markedly from those in the nondiabetic controls, except for lower left ventricular developed pressure, higher mitochondrial membrane fluidity, and protein levels of manganese superoxide dismutase. On the other hand, diabetic hearts showed significantly better post-IR functional restoration and reduced arrhythmogenesis associated with lower reactive oxygen species production as compared with healthy controls. IR decreased membrane fluidity in both experimental groups; however, it led to a complete recovery of mitochondrial Mg-ATPase activity in diabetics in contrast to its reduction in nondiabetics. These findings indicate that the heart may become adapted to diabetes-induced alterations that might increase its tolerance to an ischemic insult. Preserved mitochondrial function might play a role in the mechanisms of the heart's resistance to IR injury in diabetics.

Pemafibrate suppresses oxidative stress and apoptosis under cardiomyocyte ischemia‑reperfusion injury in type 1 diabetes mellitus

“…To determine how pemafibrate may affect the myocardial IRI under diabetic conditions, the ultrastructure of the myocardium was evaluated in the present study and marked destruction of the intracellular structures were observed in the D-IRI group. Similar alterations about myocardial injury and mitochondrial dysfunction in the diabetic IRI have been observed in other reports (25,26). In vivo analysis in the present study demonstrated that pemafibrate partially restored the mitochondrial structure in the myocardium.…”

mPTP Proteins Regulated by Streptozotocin-Induced Diabetes Mellitus Are Effectively Involved in the Processes of Maintaining Myocardial Metabolic Adaptation

“…These findings point to respiratory-chain damage as a result of the metabolic consequences of diabetes. On the other hand, in the acute phase of diabetes, experimental animals exhibited decreased vulnerability to ischemia [49], reperfusion injury [50,51], and calcium overload [52]. The latter finding was attributed to the increased rigidity of the sarcolemmal membrane due to intensified non-enzymatic glycation of membrane proteins, which decreases the mobility of membrane components and affects the permeability properties of the lipid bilayers.…”

Risk Factors of Ischemia Reperfusion Injury After PCI in Patients with Acute ST-Segment Elevation Myocardial Infarction and its Influence on Prognosis

“…Therefore, compared with STEMI patients with DM, patients without DM have stronger reaction to acute ischemic injury and are more prone to IRI ( 11 ). Muráriková’ s team believed that because the heart of DM patients may adapt to the changes caused by DM and increase tolerance to ischemic injury, the recovery of DM patients after IRI is better than that of patients without DM, with fewer cardiovascular events ( 12 ). However, there are also different research results on the relationship between DM and IRI in clinic.…”