PROTEINS AND PHOSPHOLIPIDS IN BAL FROM PATIENTS WITH HYDROSTATIC PULMONARY-EDEMA

Citation
G. Nakos et al., PROTEINS AND PHOSPHOLIPIDS IN BAL FROM PATIENTS WITH HYDROSTATIC PULMONARY-EDEMA, American journal of respiratory and critical care medicine, 155(3), 1997, pp. 945-951
Citations number
49
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
155
Issue
3
Year of publication
1997
Pages
945 - 951
Database
ISI
SICI code
1073-449X(1997)155:3<945:PAPIBF>2.0.ZU;2-0
Abstract
The purpose of the present study is twofold: to evaluate alterations i n total phospholipid content and individual phospholipid classes of th e surfactant, and to detect markers of inflammatory reaction in bronch oalveolar lavage (BAL) from patients with hydrostatic pulmonary edema (HPE). Mechanically ventilated patients with HPE (Group 1) were compar ed with mechanically ventilated patients without cardiopulmonary disea se (Group 2), considered as the control group. Group 3, including pati ents with high-permeability pulmonary edema, was used for further comp arison. BAL was obtained and immediately cooled at 4 degrees C. Total proteins, albumin, and platelet-activating factor-acetylhydrolase (PAF -AcH) were measured. Total lipids were extracted and analyzed after th in-layer chromatographic separation. PAF was determined with bioassay. Total BAL proteins and albumin were found significantly higher in pat ients with HPE compared with control, but were lower compared with adu lt respiratory distress syndrome (ARDS). PAF was elevated in patients with HPE and ARDS, whereas in the control group it was actually in non detectable levels. PAF was significantly higher in ARDS than in HPE pa tients. BAL neutrophils concentration was higher in HPE compared with control, but lower compared with ARDS. There was an inverse correlatio n between PAF-AcH and PAF. Quantitative reduction of total BAL phospho lipids (PL) and qualitative deficiency was observed in both patients w ith HPE and ARDS. The findings of this study suggest that there is evi dence of inflammation in the airspaces of patients with HPE.