The influence of liposome-encapsulated prostaglandin E-1 on hydrogen peroxide concentrations in the exhaled breath of patients with the acute respiratory distress syndrome

Citation
So. Heard et al., The influence of liposome-encapsulated prostaglandin E-1 on hydrogen peroxide concentrations in the exhaled breath of patients with the acute respiratory distress syndrome, ANESTH ANAL, 89(2), 1999, pp. 353-357
Citations number
30
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIA AND ANALGESIA
ISSN journal
00032999 → ACNP
Volume
89
Issue
2
Year of publication
1999
Pages
353 - 357
Database
ISI
SICI code
0003-2999(199908)89:2<353:TIOLPE>2.0.ZU;2-V
Abstract
Hydrogen peroxide (H2O2) levels are increased in the exhaled breath of pati ents with the acute respiratory distress syndrome (ARDS). Because liposome- encapsulated prostaglandin E-1 (PGE(1)) downregulates the CD11/CD18 recepto r of the neutrophil, thereby limiting endothelial adhesion, the use of this drug should decrease the excretion of H2O2 in the expiratory condensate of patients with ARDS. Patients >11 yr of age with ARDS (diffuse, patchy infi ltrates by chest radiograph; Pao(2)/fraction of inspired oxygen [P/F] ratio less than or equal to 200 mm Hg; pulmonary capillary wedge pressure less t han or equal to 18 mm Hg; and the requirement for mechanical ventilation) w ere randomized to receive placebo (n = 14) or escalating doses (0.15-3.6 mu g/kg) of liposomal PGE, (n = 14) every 6 h for up to 7 days. Condensate wa s collected every morning from the expiratory tubing that was submerged in an ice saltwater bath (-5 degrees C). H2O2 levels were measured by using a horseradish peroxidase assay. Other data collected included white blood cel l count and P/F ratios. There was no significant difference in the concentr ation of H2O2 in the expiratory condensate between the liposomal PGE(1) gro up and the control group either before (0.99 +/- 0.52 vs 0.93 +/- 0.48 mu m ol/L) or during treatment (1.04 +/- 0.45 vs 0.76 +/- 0.25 mu mol/L). Liposo mal PGE(1) treatment improved the P/F ratio and deceased the white blood ce ll count over time. Despite its ability to downregulate the CD11/CD18 neutr ophil receptor, liposomal PGE(1) did not reduce exhaled H2O2 excretion. Imp lications: White blood cells (WBC) are thought to be part of the cause of t he acute respiratory distress syndrome, a lung disease. WBC in the lung pro duce hydrogen peroxide, which is exhaled. Liposomal PGE(1) inhibits WBC fun ction but was found to have no effect in decreasing exhaled hydrogen peroxi de in patients with the acute respiratory distress syndrome.