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CRITICAL CARE AND TRAUMA

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

Stephen O. Heard, MD^*,, Karen Longtine, RN, Ildiko Toth, MD^*, Juan Carlos Puyana, MD, Bruce Potenza, MD, and Nicholas Smyrnios, MD

Departments of *Anesthesiology, Surgery, and Medicine, UMass Memorial Medical Center, University Campus, Worcester, Massachusetts

Address correspondence and reprint requests to Stephen O. Heard, MD, Department of Anesthesiology, UMass Memorial Medical Center, University Campus, 55 Lake Ave. North, Worcester, MA 01655. Address e-mail to stephen.heard{at}banyan.ummed.edu

Hydrogen peroxide (H₂O₂) 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 H₂O₂ 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 200 mm Hg; pulmonary capillary wedge pressure 18 mm Hg; and the requirement for mechanical ventilation) were randomized to receive placebo (n = 14) or escalating doses (0.15–3.6 µg/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°C). H₂O₂ 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 H₂O₂ in the expiratory condensate between the liposomal PGE₁ group and the control group either before (0.99 ± 0.52 vs 0.93 ± 0.48 µmol/L) or during treatment (1.04 ± 0.45 vs 0.76 ± 0.25 µmol/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 H₂O₂ 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.

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