M. Griese et al., SURFACTANT SUBFRACTIONS DURING NOSOCOMIAL INFECTION IN VENTILATED PRETERM HUMAN NEONATES, American journal of respiratory and critical care medicine, 153(1), 1996, pp. 398-403
Citations number
32
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
Long after resolution of the neonatal respiratory distress syndrome, d
eterioration of respiratory function in ventilated premature infants d
uring severe nosocomial infections is commonly observed. Based on an i
ncreased oxygen demand and ventilatory sup port, impairment of the pul
monary surfactant system was hypothesized to occur. The clinical cours
e of 10 premature neonates (764 +/- 57 gl 26.6 +/- 0.4 wk) with nosoco
mial infection mainly due to Staphylococcus epidermidis was divided in
to 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 spec
imens were obtained by small volume lavage (1 ml/kg bw), pooled to yie
ld appropriate amounts for differential centrifugation into two distin
ct subfractions known as large surfactant aggregates (LA) and small su
rfactant aggregates (SA). ''Before deterioration'' the amount of phosp
holipids recovered was constant, and the two fractions were characteri
zed by electron microscopic morphology and biochemical analysis. In th
e LA fraction lamellar body-like lipid structures were demonstrated, a
nd the phospholipid composition was typical of pulmonary surfactant in
premature neonates with a high content of phosphatidylcholine and pho
sphatidylinositol. With ''deterioration'' and ''peak'' the masses of t
otal phospholipids and of phosphatidylcholine recovered were reduced (
p < 0.05). At the same time the mass ratio of SA/LA for phosphatidylch
oline 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 c
omposition in the LA fraction did not change during the course of noso
comial infection. In the SA fraction a decrease of phosphatidylcholine
and a concomitant increase in lysophosphatidylcholine were observed a
t the ''peak'' of the infection. We concluded that, in ventilated prem
ature neonates during nosocomial infection and respiratory deteriorati
on, changes in phospholipid subfractions occur, possibly indicating im
pairment of pulmonary surfactant metabolism. These findings may be imp
ortant when considering treatment of acute lung injury with nebulized
exogenous surfactant.