title: Surfactant alterations in acute inflammatory lung injury from aspiration of acid and gastric particulates.
abstract: This study examines surfactant dysfunction in rats with inflammatory lung injury from intratracheal instillation of hydrochloric acid (ACID, pH 1.25), small nonacidified gastric particles (SNAP), or combined acid and small gastric particles (CASP). Rats given CASP had the most severe lung injury at 6, 24, and 48 h based on decreases in arterial oxygenation and increases in erythrocytes, total leukocytes, neutrophils, total protein, and albumin in bronchoalveolar lavage (BAL). The content of large surfactant aggregates in BAL was reduced in all forms of aspiration injury, but decreases were greatest in rats given CASP. Large aggregates from aspiration-injured rats also had decreased levels of phosphatidylcholine (PC) and increased levels of lyso-PC and total protein compared with saline controls (abnormalities for CASP were greater than for SNAP or ACID alone). The surface tension-lowering ability of large surfactant aggregates on a bubble surfactometer was impaired in rats with aspiration injury at 6, 24, and 48 h, with the largest activity reductions found in animals given CASP. There were strong statistical correlations between surfactant dysfunction (increased minimum surface tension and reduced large aggregate content) and the severity of lung injury based on arterial oxygenation and levels of albumin, protein, and erythrocytes in BAL (P < 0.0001). Surfactant dysfunction also correlated strongly with reduced lung volumes during inflation and deflation (P = 0.0004-0.005). These results indicate that surfactant abnormalities are functionally important in gastric aspiration lung injury and contribute significantly to the increased severity of injury found in CASP compared with ACID or SNAP alone.
authors.affiliation: Departments of Anesthesiology,University at Buffalo-State University of New York, Buffalo, NY 14214, USA.
authors.forename: Bruce A
authors.initials: BA
authors.lastname: Davidson
authors.forename: Paul R
authors.initials: PR
authors.lastname: Knight
authors.forename: Zhengdong
authors.initials: Z
authors.lastname: Wang
authors.forename: Patricia R
authors.initials: PR
authors.lastname: Chess
authors.forename: Bruce A
authors.initials: BA
authors.lastname: Holm
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Russo
authors.forename: Alan
authors.initials: A
authors.lastname: Hutson
authors.forename: Robert H
authors.initials: RH
authors.lastname: Notter
mesh_terms: D000208:Acute Disease; D000818:Animals; D018893:Bronchoalveolar Lavage; D004912:Erythrocytes / Q000378:metabolism; D005744:Gastric Acid; D006851:Hydrochloric Acid / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D007962:Leukocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008168:Lung / Q000276:immunology* / Q000473:pathology; D055370:Lung Injury; D008297:Male; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D010100:Oxygen / Q000378:metabolism; D010713:Phosphatidylcholines / Q000378:metabolism; D011015:Pneumonia, Aspiration / Q000276:immunology* / Q000473:pathology; D011506:Proteins / Q000378:metabolism; D011651:Pulmonary Artery / Q000378:metabolism; D011663:Pulmonary Surfactants / Q000032:analysis / Q000378:metabolism*; D051381:Rats; D020318:Rats, Long-Evans; D013500:Surface Tension
chemical_list: D018836:Inflammation Mediators; D010713:Phosphatidylcholines; D011506:Proteins; D011663:Pulmonary Surfactants; D006851:Hydrochloric Acid; D010100:Oxygen