Surfactant alterations in severe pneumonia, acute respiratory distress syndrome, and cardiogenic lung edema.
Bronchoalveolar lavage fluids (BALF) were analyzed for surfactant abnormalities in 153 patients with acute respiratory failure necessitating mechanical ventilation. Diagnoses were acute respiratory distress syndrome (ARDS) in the absence of lung infection (n = 16), severe pneumonia (PNEU; n = 88), ARDS and PNEU (n = 36), and cardiogenic lung edema (CLE; n = 13). The PNEU group was subdivided into groups with alveolar PNEU (n = 35), bronchial PNEU (n = 16), interstitial PNEU (n = 18) and nonclassified PNEU (n = 19). Comparison with healthy controls (n = 20) was undertaken. Total phospholipids (PL), proteins, PL classes (HPTLC) and surfactant apoproteins SP-A and SP-B (ELISA) were quantified in the original BALF. The 48,000 x g pellet from centrifugation of the BAL was used to assess the percentage of large surfactant aggregates (LSA) and the biophysical properties of the surfactant (pulsating bubble surfactometer). All groups with inflammatory lung injury (PNEU and/or ARDS) showed some decrease in the lavageable PL pool, a reduced LSA content in BALF, and a manifold increase in alveolar protein load. Marked changes in the PL profile were noted throughout the groups (a decrease in phosphatidylcholine (PC) and phosphatidylglycerol (PG) and an increase in phosphatidylinositol [PI] and sphingomyelin [SPH]). Concentrations of SP-A but not of SP-B in BALF were reduced. Minimum surface-tension values approached 0 mN/m in controls, and ranged from 10 to 25 mN/m in the absence of supernatant protein and from 20 to 35 mN/m in recombination with leaked protein in the groups with ARDS and/or PNEU. Abnormalities in alveolar PNEU surpassed those in bronchial PNEU, and interstitial PNEU presented a distinct pattern with extensive metabolic changes. All surfactant changes were absent in CLE except for a slight inhibition of surface activity by proteins. We conclude that pronounced surfactant abnormalities, comparable to those in ARDS in the absence of lung infection, occur in different entities of severe PNEU, but not in CLE.
Günther
A
A
Department of Internal Medicine, Justus-Liebig-University, Giessen, Germany.
Siebert
C
C
Schmidt
R
R
Ziegler
S
S
Grimminger
F
F
Yabut
M
M
Temmesfeld
B
B
Walmrath
D
D
Morr
H
H
Seeger
W
W
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D001059:Apoproteins / Q000032:analysis; D001669:Biochemical Phenomena; D001671:Biochemistry; D055592:Biophysical Phenomena; D001703:Biophysics; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry* / Q000166:cytology; D002452:Cell Count; D003627:Data Interpretation, Statistical; D006333:Heart Failure / Q000150:complications; D006801:Humans; D008875:Middle Aged; D010743:Phospholipids / Q000032:analysis; D011014:Pneumonia / Q000175:diagnosis*; D011654:Pulmonary Edema / Q000175:diagnosis* / Q000209:etiology; D011663:Pulmonary Surfactants / Q000032:analysis*; D012128:Respiratory Distress Syndrome / Q000175:diagnosis*; D013500:Surface Tension
D001059:Apoproteins; D010743:Phospholipids; D011663:Pulmonary Surfactants