SURFACTANT SUBFRACTIONS DURING NOSOCOMIAL INFECTION IN VENTILATED PRETERM HUMAN NEONATES

Citation
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
ISSN journal
1073449X
Volume
153
Issue
1
Year of publication
1996
Pages
398 - 403
Database
ISI
SICI code
1073-449X(1996)153:1<398:SSDNII>2.0.ZU;2-S
Abstract
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.