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Updated: Mar 25, 2026
A Recovery Cardiopulmonary Bypass Model Without Transfusion or Inotropic Agents in Rats
Published on: March 23, 2018
Effects of cardiopulmonary bypass on lung nuclear factor-kappa B activity, cytokine release, and pulmonary function
Gaisheng Yang1, Xiaodong Xue1, Yanying Chen1
1Department of Anesthesiology, Airforce General Hospital, Beijing 100142, China.
Objectives:
To study the effect of cardiopulmonary bypass (CPB) on nuclear factor-kappa B (NF-κB) and cytokine expression and pulmonary function in dogs.
Materials And Methods:
Twelve male mongrel dogs were divided into a methylprednisolone group (group M) and a control group (group C). All animals underwent aortic and right atrial catheterization under general anesthesia. Changes in pulmonary function and hemodynamics were monitored and the injured site was histologically evaluated.
Results:
The activity of NF-κB and myeloperoxidase (MPO), levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8, and the wet/dry (W/D) weight ratio were significantly higher after CPB than before CPB in both groups (P<0.01), with the lower values in group M than in group C, at different time points (P<0.01). Histological evaluation revealed neutrophilic infiltration and thickening of the alveolar interstitium in both groups; however, the degree of pathological changes was significantly lower in group M than in group C. The alveolar-arterial O2 tension difference (PA-aDO2) was significantly higher after CPB than before CBP (P<0.01), and lower in group M than in group C (P<0.01). The pulmonary compliance after removal of the aortic clamp obviously decreased in group C (P<0.05), with no significant change in group M.
Conclusion:
CPB can significantly enhance the activation of NF-κB in lung tissues and increase the expression of inflammatory cytokines, thus inducing lung injury. Methylprednisolone can inhibit the NF-κB activation, thus inhibiting the release of cytokines and protecting the lung function.
