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Surfactant dysfunction is a primary pathophysiologic component in patients with adult respiratory distress syndrome (ARDS). In this study we tested the efficacy of aerosolized surfactant (Sf ) replacement in a severe lung injury model of endotoxin-induced ARDS. Twenty-one certified healthy pigs were anesthetized, surgically prepared for measurement of hemodynamic and lung function, then randomized into one of four groups: (1) control (n = 5), surgical instrumentation only; (2) lipopolysaccharide (LPS) (n = 6), infused with Escherichia coli LPS (100 microgram/kg) without positive end- expiratory pressure (PEEP) and ventilated with a nonhumidified gas mixture of 50% N2O and 50% O2; (3) LPS + PEEP (n = 4), infused with LPS, placed on PEEP (7.5 cm H2O), and ventilated with a humidified gas mixture; and (4) LPS + PEEP + Sf (n = 6), infused with LPS, placed on PEEP, and ventilated with aerosolized Sf (Infasurf, ONY, Inc.). All animals were studied for 6 h. Arterial PO2 significantly decreased in both the LPS and LPS + PEEP groups (LPS + PEEP = 74 +/- 19 mm Hg; LPS = 74 +/- 19 mm Hg, p < 0.05) while venous admixture (Q S/Q T) increased in these groups (LPS + PEEP = 43.3 +/- 3.9%; LPS = 47.7 +/- 11%, p < 0.05) as compared with the control group. PEEP + Sf reduced the fall in PO2 (142 +/- 20 mm Hg) and rise in Q S/Q T (15.1 +/- 3.6%) caused by LPS. Delayed induction of PEEP (2 h following LPS) did not significantly improve any parameter over the LPS group without PEEP in this ARDS model. LPS without PEEP (3.4 +/- 0.2 cells/6,400 micrometer2) caused a marked increase in the total number of sequestered leukocytes in the pulmonary parenchyma as compared with the control group (1.3 +/- 0.1 cells/6,400 micrometer2). LPS + PEEP + Sf (2.3 +/- 0.2 cells/6,400 micrometer2) significantly decreased while LPS + PEEP significantly increased (4.0 +/- 0.2 cells/6,400 micrometer2) the total number of sequestered leukocytes as compared with the LPS without PEEP group. In summary, aerosolized surfactant replacement decreased leukocyte sequestration and improved oxygenation in our porcine model of endotoxin-induced lung injury.
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
January 2004,
Lung,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
June 2020,
International journal of pharmaceutics,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
March 1996,
Critical care medicine,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
October 1987,
European journal of respiratory diseases,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
January 2009,
Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
August 1999,
Biochimica et biophysica acta,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
August 2006,
Vascular pharmacology,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
December 2002,
American journal of respiratory and critical care medicine,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
January 2005,
Experimental lung research,
C Lutz, and
D Carney, and
C Finck, and
A Picone, and
L A Gatto, and
A Paskanik, and
E Langenback, and
G Nieman
December 2006,
Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue,
