• Xue Yang, Jianjiang Wu, Hu Cheng, Siyu Chen, and Jiang Wang.
• Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
• Shock. 2023 Nov 1; 60 (5): 678687678-687.

AbstractObjective: Neurological complications after myocardial ischemia/reperfusion (IR) injury remain high and seriously burden patients and their families. Dexmedetomidine (Dex), an α 2 agonist, is endowed with analgesic-sedative and anti-inflammatory effects. Therefore, our study aims to explore the mechanism and effect of Dex on brain damage after myocardial IR injury. Methods C57BL/6 mice were randomly divided into sham, IR, and IR + Dex groups, and myocardial IR models were established. The impact of Dex on brain injury elicited by myocardial IR was assessed via ELISA for inflammatory factors in serum and brain; Evans blue for blood-brain barrier permeability; hematoxylin-eosin staining for pathological injury in brain; immunofluorescence for microglia activation in brain; Morris water maze for cognitive dysfunction; western blot for the expression level of HIF-1α, occludin, cleaved caspase-3, NF-κB p65, and p-NF-κB p65 in the brain. In addition, HIF-1α knockout mice were used to verify whether the neuroprotective function of Dex is associated with the HIF-1 pathway. Results: Dex was capable of reducing myocardial IR-induced brain damage including inflammatory factor secretion, blood-brain barrier disruption, neuronal edema, microglial activation, and acute cognitive dysfunction. However, the protective role of Dex was attenuated in HIF-1α knockout mice. Conclusion: Dex protects against myocardial IR-induced brain injury, and the neuroprotection of Dex is at least partially dependent on the activation of the HIF-1 pathway.Copyright © 2023 by the Shock Society.

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