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Fig. 1 | BMC Anesthesiology

Fig. 1

From: Postoperative remote lung injury and its impact on surgical outcome

Fig. 1

Molecular mechanisms of remote lung injury following other organ injury or disease conditions. Key cytokines involved in lung injury are IL-6, IL-8 and TNF-α, which are induced by acute kidney injury (AKI), cardiopulmonary bypass, renal ischaemia-reperfusion injury, bilateral nephrectomy, transfusion-related acute lung injury and mechanical ventilation. Ischaemic AKI triggers the production of TNF-α which, upon binding to TNFR1, results in NF-κB activation and pulmonary apoptosis. Epithelial cell apoptosis is caspase-3 dependent and can occur following AKI, haemorrhagic shock, sepsis, hepatopulmonary syndrome, acute liver disease and cardiopulmonary bypass, while capillary endothelial cell apoptosis is independent of caspase. Pulmonary epithelial or capillary endothelial cell apoptosis leads to alveolar-capillary barrier dysfunction, causing the accumulation of protein rich fluid in alveoli and subsequent pulmonary oedema. HMGB1 binds to TLR4, leading to the activation of NAD(P) H oxidase in neutrophils, release of ROS, neutrophil infiltration and pulmonary oedema. Derangement of the alveolar capillary barrier causes the release of cytokines and chemokines, facilitating further neutrophil recruitment and the subsequent release of proteases, ROS and cytokines which further damage the barrier and worsen pulmonary oedema (Modified and reproduced with permission) (Springer Nature; Nature Reviews Nephrology) [13]

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