The cardioprotective effect of dexmedetomidine on regional ischemia/reperfusion injury in type 2 diabetic rat hearts.

BACKGROUND

Dexmedetomidine (DEX) is an α2-adrenergic receptor agonist commonly used during perioperative periods due to its sedation and analgesia effect. It is confirmed that DEX has cardioprotective effects against ischemia/reperfusion (I/R) injury. We investigated whether DEX administration is beneficial to type 2 diabetic rats subjected to I/R injury.

METHODS

The diabetes model was established by providing a high-fat diet for 2 weeks followed by injecting 35 mg/kg streptozotocin (STZ). The myocardial I/R model consisted of left anterior descending coronary artery occlusion for 30 min followed by reperfusion for two-hours. DEX was administered before ischemia; alternatively, yohimbine was administered with or without DEX before ischemia. At the end of reperfusion, the rats were sacrificed, and hearts were isolated for histology. The levels of glycogen synthase kinase-3β (GSK-3β) and phosphorylated GSK-3β (p-GSK-3β) were quantitatively analyzed. The infarct size was measured via Evans Blue and 2,3,5‑triphenyltetrazolium chloride (TTC) staining. Plasma samples were collected to measure the levels of cardiac Troponin T (cTnT). Arrhythmia scores were recorded during the first few minutes of reperfusion.

RESULTS

DEX preconditioning significantly reduced myocardial infarct size, arrhythmia scores and the plasma cTnT levels, and increased the p-GSK-3β levels. All of these protective effects of DEX were reversed by co-administration of yohimbine.

CONCLUSIONS

These results suggested that DEX preconditioning exerted a cardioprotective effect against regional I/R injury in diabetic rats.