The Influence of Liposome-Encapsulated Prostaglandin E1 on Hydrogen Peroxide Concentrations in the Exhaled Breath of Patients with the Acute Respiratory Distress Syndrome

Abstract

Hydrogen peroxide (H2 O2) levels are increased in the exhaled breath of patients with the acute respiratory distress syndrome (ARDS).Because liposome-encapsulated prostaglandin E1 (PGE1) downregulates the CD11/CD18 receptor of the neutrophil, thereby limiting endothelial adhesion, the use of this drug should decrease the excretion of H2 O2 in the expiratory condensate of patients with ARDS. Patients >11 yr of age with ARDS (diffuse, patchy infiltrates by chest radiograph; PaO2/fraction of inspired oxygen [P/F] ratio <or=to200 mm Hg; pulmonary capillary wedge pressure <or=to18 mm Hg; and the requirement for mechanical ventilation) were randomized to receive placebo (n = 14) or escalating doses (0.15-3.6 [micro sign]g/kg) of liposomal PGE1 (n = 14) every 6 h for up to 7 days. Condensate was collected every morning from the expiratory tubing that was submerged in an ice saltwater bath (-5[degree sign]C). H2 O2 levels were measured by using a horseradish peroxidase assay. Other data collected included white blood cell count and P/F ratios. There was no significant difference in the concentration of H2 O2 in the expiratory condensate between the liposomal PGE1 group and the control group either before (0.99 +/- 0.52 vs 0.93 +/- 0.48 [micro sign]mol/L) or during treatment (1.04 +/- 0.45 vs 0.76 +/- 0.25 [micro sign]mol/L). Liposomal PGE1 treatment improved the P/F ratio and decreased the white blood cell count over time. Despite its ability to downregulate the CD11/CD18 neutrophil receptor, liposomal PGE1 did not reduce exhaled H2 O2 excretion. Implications: White blood cells (WBC) are thought to be part of the cause of the acute respiratory distress syndrome, a lung disease. WBC in the lung produce hydrogen peroxide, which is exhaled. Liposomal PGE1 inhibits WBC function but was found to have no effect in decreasing exhaled hydrogen peroxide in patients with the acute respiratory distress syndrome. (Anesth Analg 1999;89:353-7)