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A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration
Published on: February 27, 2018
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Prolonged mechanical ventilation-induced neuroinflammation affects postoperative memory dysfunction in surgical mice.
Chang Chen1, Zongze Zhang2, Ting Chen3
1Department of Anesthesiology, Zhongnan Hospital, Wuhan University, East Lake Road, Wuhan, 430071, Hubei, China. chang-dream@126.com.
Critical Care (London, England)
|April 19, 2015
Summary
Prolonged mechanical ventilation (MV) after surgery worsens memory deficits in mice. This cognitive decline is linked to increased inflammation and cellular damage in the hippocampus.
Area of Science:
- Neuroscience
- Surgical Research
- Inflammation Biology
Background:
- Postoperative cognitive dysfunction is a common complication.
- Mechanical ventilation (MV) may impact acute brain outcomes after surgery.
Purpose of the Study:
- To investigate the effect of prolonged mechanical ventilation (MV) on postoperative memory dysfunction in surgical mice.
- To explore the underlying mechanisms involving inflammation and cellular damage.
Main Methods:
- Male C57BL/6 mice underwent surgery and were divided into control, surgery-only, and MV groups for varying durations (1, 3, 6 hours).
- Memory function was assessed using fear conditioning tests.
- Systemic and hippocampal inflammatory markers (IL-1β, IL-6, TNFα), synaptic structure, microglial activation, and apoptotic markers were analyzed.
Main Results:
- Prolonged MV (6 hours) led to synapse degeneration, increased apoptosis markers (cytochrome c, cleaved caspase-3, cleaved PARP-1), and reduced memory performance (decreased freezing time).
- MV induced significant increases in NF-κB activation and levels of IL-1β, IL-6, and TNFα in both systemic circulation and the hippocampus.
Conclusions:
- Prolonged mechanical ventilation exacerbates postoperative cognitive decline.
- This effect is associated with increased hippocampal inflammation (IL-1β, IL-6, TNFα) and glial cell activation.
