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Pressure Controlled Ventilation to Induce Acute Lung Injury in Mice
Published on: May 5, 2011
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Sevoflurane attenuates ventilator‑induced lung injury by regulating c‑PLA2 expression
Yong Yang1, Wen-Fa Wang2, Yan-Hua Li3
1Experimental Center of Medical Function, Kunming Medical University, Kunming, Yunnan 650031, P.R. China.
Molecular Medicine Reports
|July 18, 2018
Summary
One-lung ventilation (OLV) promotes lung inflammation via the club cell secretory protein (CCSP) and cytosolic phospholipase A2 (c-PLA2) pathway. Sevoflurane may offer protection independent of CCSP.
Area of Science:
- Anesthesiology
- Pulmonary Medicine
- Cell Biology
Background:
- Pulmonary inflammation is a significant concern during one-lung ventilation (OLV).
- Club cell secretory protein (CCSP) is an endogenous modulator of lung inflammation.
- The role of CCSP in sevoflurane-induced pulmonary inflammation during OLV requires clarification.
Purpose of the Study:
- To investigate the role of CCSP in sevoflurane-induced pulmonary inflammation during OLV.
- To elucidate the pathway involving CCSP and cytosolic phospholipase A2 (c-PLA2) in lung injury.
Main Methods:
- Rabbits underwent sham operation, OLV, or OLV with sevoflurane, with or without club cell exfoliation.
- Lung injury was assessed via wet/dry weight ratio and histology.
- mRNA and protein expression of CCSP and c-PLA2 were measured.
- Arachidonic acid levels were determined by ELISA.
Main Results:
- OLV increased lung injury, c-PLA2 expression, and decreased CCSP expression.
- Sevoflurane inhalation during OLV upregulated CCSP and downregulated c-PLA2.
- Club cell exfoliation exacerbated OLV-induced lung injury and c-PLA2 expression.
- Sevoflurane mitigated lung injury and c-PLA2 expression even after club cell exfoliation.
Conclusions:
- OLV promotes lung inflammation through the CCSP and c-PLA2 pathway.
- Sevoflurane exerts a protective effect against OLV-induced lung injury.
- CCSP may not be essential for the protective effect of sevoflurane.
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