Mediators of septic lung injury.
Septic pulmonary injury remains a significant cause of morbidity and mortality among hospitalized patients today and is likely to increase in prevalence as advances in medical technology allow the salvage of more critically ill and immunocompromised hosts. Treatment of the host's underlying disease and even of the infection itself has appeared to redeem septic patients only to have them succumb in increasing numbers to the pulmonary injury reaction. Our understanding of the mechanisms and mediators of lung dysfunction in sepsis is in a rapidly expanding phase. Currently we recognize the contributions of several blood elements, lipids, and peptides to pulmonary injury, although the relative importance and points of interaction and interdependence of these mediators remain to be established. It is hoped that a more complete understanding of the process of pulmonary injury in sepsis will suggest effective means of intervention at a stage in which damage may be reversed or minimized.
D000818:Animals; D002449:Cell Aggregation; D003165:Complement System Proteins / Q000276:immunology; D005337:Fibrin / Q000502:physiology; D006801:Humans; D007975:Leukotriene B4 / Q000502:physiology; D008168:Lung / Q000503:physiopathology; D009504:Neutrophils / Q000276:immunology / Q000502:physiology; D010974:Platelet Aggregation; D011453:Prostaglandins / Q000502:physiology; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000503:physiopathology; D013189:SRS-A / Q000502:physiology; D018805:Sepsis / Q000150:complications* / Q000503:physiopathology
D011453:Prostaglandins; D013189:SRS-A; D007975:Leukotriene B4; D005337:Fibrin; D003165:Complement System Proteins