Am. J. Respir. Crit. Care Med., Vol 153, No. 1, 01 1996, 398-403.
Surfactant subfractions during nosocomial infection in ventilated preterm human neonates
M Griese, P Dietrich, C Potz, B Westerburg, R Bals and D Reinhardt
Lung Research Group, Kinderpoliklinik, Ludwig-Maximilians University, Munich, Germany.
Long after resolution of the neonatal respiratory distress syndrome,
deterioration of respiratory function in ventilated premature infants
during severe nosocomial infections is commonly observed. Based on an
increased oxygen demand and ventilatory support, impairment of the
pulmonary surfactant system was hypothesized to occur. The clinical course
of 10 premature neonates (764 +/- 57 g, 26.6 +/- 0.4 wk) with nosocomial
infection mainly due to Staphylococcus epidermidis was divided into four
periods in each individual patient: "before deterioration" (average 8 to 11
d of life), "deterioration" (11 to 17 d), "peak" (17 to 22 d), and
"recovery" (22 to 24 d). A total of 810 airway specimens were obtained by
small volume lavage (1 ml/kg bw), pooled to yield appropriate amounts for
differential centrifugation into two distinct subfractions known as large
surfactant aggregates (LA) and small surfactant aggregates (SA). "Before
deterioration" the amount of phospholipids recovered was constant, and the
two fractions were characterized by electron microscopic morphology and
biochemical analysis. In the LA fraction lamellar body-like lipid
structures were demonstrated, and the phospholipid composition was typical
of pulmonary surfactant in premature neonates with a high content of
phosphatidylcholine and phosphatidylinositol. With "deterioration" and
"peak" the masses of total phospholipids and of phosphatidylcholine
recovered were reduced (p < 0.05). At the same time the mass ratio of
SA/LA for phosphatidylcholine decreased from 0.32 +/- 0.10 to 0.18 +/-
0.03, indicating a more pronounced decrease of the SA fraction (p <
0.05). The phospholipid composition in the LA fraction did not change
during the course of nosocomial infection. In the SA fraction a decrease of
phosphatidylcholine and a concomitant increase in lysophosphatidylcholine
were observed at the "peak" of the infection. We concluded that, in
ventilated premature neonates during nosocomial infection and respiratory
deterioration, changes in phospholipid subfractions occur, possibly
indicating impairment of pulmonary surfactant metabolism. These findings
may be important when considering treatment of acute lung injury with
nebulized exogenous surfactant.
