急性呼吸窘迫综合征
医学
肺
呼吸窘迫
肺水肿
弥漫性肺泡损伤
炎症
麻醉
病理
免疫学
内科学
急性呼吸窘迫
作者
Sarah de Oliveira Rodrigues,Matheus Augusto Patricio de Almeida,Hugo C. Castro‐Faria‐Neto,Adriana Ribeiro Silva,Cassiano Felippe Gonçalves-de-Albuquerque
摘要
Acute respiratory distress syndrome (ARDS) is a significant threat to critically ill patients with a high fatality rate. Pollutant exposure, cigarette smoke, infectious agents, and fatty acids can induce ARDS. Animal models can mimic the complex pathomechanism of the ARDS. However, each of them has limitations. Notably, oleic acid (OA) is increased in critically ill patients with harmful effects on the lung. OA can induce lung injury by emboli, disrupting tissue, altering pH, and impairing edema clearance. OA-induced lung injury model resembles various features of ARDS with endothelial injury, increased alveolar permeability, inflammation, membrane hyaline formation, and cell death. Herein, induction of lung injury is described by injecting OA (in salt form) directly into the lung and intravenously in a mouse since it is the physiological form of OA at pH 7. Thus, the injection of OA in the salt form is a helpful animal model to study lung injury/ARDS without causing emboli or altering the pH, thereby getting close to what is happening in critically ill patients.
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