Cytoprotection of heme oxygenase-1/carbon monoxide in lung injury.
Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) have been the major cause of morbidity and mortality in intensive care units (ICU) over the past decades despite advances in therapeutic modalities. This syndrome is characterized by noncardiogenic pulmonary edema, and pulmonary and systemic inflammation resulting in respiratory failure (1, 2). Both exudative and proliferative organizing phases of ARDS/ALI have been described pathologically (3, 4). The exudative phase is often called diffuse alveolar damage (DAD) characterized by inflammation and hyaline membrane composed of fibrin and cellular debris (3--5). Pulmonary alveolar cell death is the major pathologic change during the exudative phase in DAD. Repair and remodeling of injured lung cells occur during the proliferative phase, characterized by hyperplasia of alveolar type II cells and fibroblast proliferation (3-5). A variety of cellular insults can cause ALI/ARDS including but not limited to sepsis, trauma, drugs, high concentration of oxygen therapy, and mechanical ventilation (1, 2, 5). The broad spectrum of insults that potentially cause ARDS highlights the complexity of pathogenesis of this syndrome.
Jin
Yang
Y
Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Choi
Augustine M K
AM
D000818:Animals; D017209:Apoptosis; D002248:Carbon Monoxide / Q000502:physiology*; D051547:Heme Oxygenase-1 / Q000502:physiology*; D006801:Humans; D012128:Respiratory Distress Syndrome / Q000503:physiopathology*
D002248:Carbon Monoxide; D051547:Heme Oxygenase-1