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Dexmedetomidine improved one-lung ventilation-induced cognitive dysfunction in rats.

Mengyun Li1, Zhe Jin1, Jia Zhan1

  • 1Department of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, PR China.

BMC Anesthesiology
|April 23, 2022
PubMed
Summary

Dexmedetomidine (DEX) improved cognitive function and reduced brain oxygen consumption in rats during one-lung ventilation (OLV). DEX also protected synaptic structures and activated the ERK1/2-CREB pathway.

Keywords:
CERO2Cognitive DysfunctionDexmedetomidineERK1/2-CREB-Bcl-2One-Lung Ventilation

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Area of Science:

  • Anesthesiology
  • Neuroscience
  • Thoracic Surgery

Background:

  • One-lung ventilation (OLV) is a common procedure in thoracic surgery.
  • OLV can increase cerebral oxygen consumption (CERO2) and impair cognitive recovery.
  • The neuroprotective effects of dexmedetomidine (DEX) during OLV require further investigation.

Purpose of the Study:

  • To investigate the impact of dexmedetomidine (DEX) on cognitive function in rats subjected to one-lung ventilation (OLV).
  • To assess DEX's effects on cerebral oxygen consumption, synaptic structure, and relevant molecular pathways.

Main Methods:

  • Sprague-Dawley rats were divided into two-lung ventilation (TLV), OLV, and DEX-treated OLV groups.
  • DEX was administered intraperitoneally 30 minutes before induction.
  • Cognitive function was evaluated using the Morris water maze (MWM) test.
  • Western blotting and transmission electron microscopy (TEM) were used to analyze hippocampal tissues.

Main Results:

  • DEX administration improved spatial memory in the MWM test compared to the OLV group.
  • DEX reduced cerebral oxygen consumption (CERO2) and protected synaptic structures in the hippocampal CA1 region.
  • DEX upregulated the expression of pERK1/2, pCREB, and Bcl-2, while decreasing BAX expression.

Conclusions:

  • Dexmedetomidine (DEX) administration enhances post-operative cognitive function in rats undergoing one-lung ventilation (OLV).
  • DEX reduces cerebral oxygen consumption and preserves synaptic integrity.
  • The neuroprotective effects of DEX are associated with the upregulation of the ERK1/2-CREB anti-apoptotic signaling pathway.