A young metastatic lung cancer patient developed empyema due to an infection with carbapenem-resistant Acinetobacter baumannii. Hydropneumothorax was detected and managed by a tube thoracotomy. However, persistent air leakage through the chest tube was observed due to the presence of a bronchopleural fistula (BPF). As hypercapnic respiratory failure had progressed and the large air leak did not diminish by conservative management, a pumpless extracorporeal lung assist (pECLA) device was inserted. The pECLA allowed the patient to be weaned from mechanical ventilation and the BPF to heal. The present case shows the effective application of pECLA in a patient with empyema complicated with BPF and severe hypercapnic respiratory failure. pECLA enabled us to minimize airway pressure to aid in the closure of the BPF in the mechanically ventilated patient.
Background Arginine vasopressin (AVP) is widely used as a vasopressor agent. Some recent studies have suggested that AVP may exert an immunomodulatory effect. However, the mechanism about the anti-inflammatory effect of AVP is not well known. We investigated the effect of AVP on the ihibitor of kappa B (IκBα)/nuclear factor-kappa B (NF-κB) pathway in RAW 264.7 cells.
Methods Cultured RAW 264.7 cells were pretreated with AVP and stimulated with lipopolysaccharide (LPS). To evaluate the effect of AVP on inflammatory cytokines, the concentration of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were assessed by an enzyme-linked immunosorbent assay technique. The expression of IκBα and nuclear translocation of NF-κB p65 were measured by Western blotting, and IκB kinase (IKK) activity was analyzed by an in vitro immune complex kinase assay. To confirm the AVP effect on IκBα/NF-κB cascade and via V2 receptor, we added tolvaptan (V2 receptor antagonist) after AVP pretreatment.
Results The increase of IL-6 and TNF-α in LPS-stimulated RAW 264.7 cells was suppressed by a treatment with AVP. Pretreatment of AVP inhibited increasing of IKK activity and IκBα degradation induced by LPS in RAW 264.7 cells. Furthermore, LPS induced and NF-κB transcription was inhibited by AVP pretreatment. The observed changes in IKK activity, IκBα degradation and NF-κB transcription by AVP was abolished by tolvaptan treatment.
Conclusions Our results suggest that AVP showed anti-inflammatory effect on LPS-induced IκBα/NF-κB cascade in mouse macrophages via V2 receptors.
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