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