Effect of dexmedetomidine and cholinergic anti-inflammatory pathways in myocardial ischemia-reperfusion injury.
Youting Ju, Fan Xiao, Jun Lu, Bin Zhou, Junying Cai, Shoulin Chen
Abstract
Youting Ju, Fan Xiao, Jun Lu, Bin Zhou, Junying Cai, Shoulin Chen
Abstract
The aim of the current study was to determine the effect and mechanism underlying the cholinergic anti-inflammatory pathway of dexmedetomidine and the cholinergic anti-inflammatory pathway on myocardial ischemia-reperfusion 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 pre-treatment [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), BCL2-associated X (bax), caspase-3, α7 Nicotinic acetylcholine receptor (α-7 nR), and inhibitor of nuclear factor kappa-Bα (I-κB-α) in the myocardium was measured. Dexmedetomidine can significantly reduce the myocardial tissue injury induced by myocardial ischemia-reperfusion in rats. Dexmedetomidine may relieve myocardial ischemia-reperfusion injury by activating the cholinergic anti-inflammatory pathway.
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The aim of the current study was to determine the effect and mechanism underlying the cholinergic anti-inflammatory pathway of dexmedetomidine and the cholinergic anti-inflammatory pathway on myocardial ischemia-reperfusion 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 pre-treatment [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), BCL2-associated X (bax), caspase-3, α7 Nicotinic acetylcholine receptor (α-7 nR), and inhibitor of nuclear factor kappa-Bα (I-κB-α) in the myocardium was measured. Dexmedetomidine can significantly reduce the myocardial tissue injury induced by myocardial ischemia-reperfusion in rats. Dexmedetomidine may relieve myocardial ischemia-reperfusion injury by activating the cholinergic anti-inflammatory pathway.
Key concepts: Dexmedetomidine, Medicine, Ischemia, Reperfusion injury, Cholinergic, Anesthesia, Lactate dehydrogenase, Pharmacology