Abstract:
The aim of the current study was to determine the effect and mechanism underlying the cholinergic antiinflammatory pathway of dexmedetomidine and the cholinergic anti-inflammatory pathway on myocardial ischemiareperfusion injury by establishing a myocardial ischemia-reperfusion model in rats. Sixty healthy rats were randomly divided into 4 groups with 15 rats in each group. The first group was a sham operation group. The second group (myocardial ischemia-reperfusion model group [Ischemia-reperfusion injury (IRI)+S group]) was pre-treated with saline for 10 min before ischemia. The third group (myocardial ischemia reperfusion model with dexmedetomidine pretreatment [IRI+Dex group]) received an intravenous injection of dexmedetomidine for 10 min before ischemia. The fourth group was the myocardial ischemia reperfusion model with dexmedetomidine pre-treatment and the disconnection of the vagus nerve group (IRI+Dex+V group). The serum creatine kinase (CK) and lactate dehydrogenase (LDH) levels were determined. The expression of B cell lymphoma/lewkmia-2 (bcl-2), Nicotinic acetylcholine receptor (α-7 nR), and BCL2-associated X (bax), caspase-3, inhibitor of nuclear factor kappaBα α7 (I-κB-α) in the myocardium was measured. Dexmedetomidine can significantly reduce the myocardial tissue injury induced by myocardial ischemiareperfusion in rats. Dexmedetomidine may relieve myocardial ischemia-reperfusion injury by activating the cholinergic anti-inflammatory pathway.
