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Cytoprotection of Heme Oxygenase-1/Carbon Monoxide in Lung Injury

Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania

Correspondence and requests for reprints should be addressed to Augustine M. K. Choi, M.D., Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, MUH 628, Pittsburgh, PA 15213. E-mail: choiam{at}upmc.edu

ABSTRACT

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.

Key Words: carbon monoxide • cytoprotection • heme oxygenase • lung injury

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