[Aspiration pneumonitis; progress in understanding its acute pathophysiology and its therapy].
Aspiration of gastric contents has been a major cause of acute respiratory failure in adult patients, and its mortality has been very high. Current method of treatment is limited, but the pathogenesis of acid aspiration lung injury has been well studied. The lung injury can be divided into direct and secondary injury. Neutrophils are thought to be a primary mediator of the secondary lung and systemic organ injury. Various substances such as cytokines, complements, and arachidonic acid metabolites, which activate neutrophils, are produced in acid aspiration pneumonitis. In this article, the progress in research of the acute pathophysiology of acid aspiration pneumonitis is reviewed and the possibility of its application to therapy is discussed.
Kudoh
I
I
Department of Anesthesiology, Yokohama City University School of Medicine.
D000758:Anesthesia / Q000009:adverse effects; D000818:Animals; D001095:Arachidonic Acids / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000502:physiology; D003165:Complement System Proteins / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000209:etiology; D018375:Neutrophil Activation / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology; D011015:Pneumonia, Aspiration / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D012128:Respiratory Distress Syndrome / Q000209:etiology
D001095:Arachidonic Acids; D015815:Cell Adhesion Molecules; D016207:Cytokines; D009569:Nitric Oxide; D003165:Complement System Proteins