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dc.contributor.authorHeard, Stephen O.
dc.contributor.authorLongtine, Karen J.
dc.contributor.authorToth, Ildiko
dc.contributor.authorPuyana, Juan Carlos
dc.contributor.authorPotenza, Bruce
dc.contributor.authorSmyrnios, Nicholas A.
dc.date2022-08-11T08:09:35.000
dc.date.accessioned2022-08-23T16:36:35Z
dc.date.available2022-08-23T16:36:35Z
dc.date.issued1999-08-10
dc.date.submitted2008-02-29
dc.identifier.citation<p>Anesth Analg. 1999 Aug;89(2):353-7.</p>
dc.identifier.issn0003-2999 (Print)
dc.identifier.doi10.1213/00000539-199908000-00020
dc.identifier.pmid10439747
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38817
dc.description.abstractHydrogen 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 < or = 200 mm Hg; pulmonary capillary wedge pressure < or = 18 mm Hg; and the requirement for mechanical ventilation) were randomized to receive placebo (n = 14) or escalating doses (0.15-3.6 micrograms/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 degrees 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 mumol/L) or during treatment (1.04 +/- 0.45 vs 0.76 +/- 0.25 mumol/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.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10439747&dopt=Abstract ">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1213/00000539-199908000-00020
dc.subjectAdult
dc.subjectAlprostadil
dc.subject*Breath Tests
dc.subjectDrug Carriers
dc.subjectFemale
dc.subjectHumans
dc.subjectHydrogen Peroxide
dc.subjectInfusions, Intravenous
dc.subjectLeukocyte Count
dc.subjectLiposomes
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectRespiratory Distress Syndrome, Adult
dc.subjectAnesthesiology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectRespiratory Tract Diseases
dc.subjectSurgery
dc.titleThe influence of liposome-encapsulated prostaglandin E1 on hydrogen peroxide concentrations in the exhaled breath of patients with the acute respiratory distress syndrome
dc.typeJournal Article
dc.source.journaltitleAnesthesia and analgesia
dc.source.volume89
dc.source.issue2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1165&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/166
dc.identifier.contextkey441931
refterms.dateFOA2022-08-23T16:36:35Z
html.description.abstract<p>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 < or = 200 mm Hg; pulmonary capillary wedge pressure < or = 18 mm Hg; and the requirement for mechanical ventilation) were randomized to receive placebo (n = 14) or escalating doses (0.15-3.6 micrograms/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 degrees 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 mumol/L) or during treatment (1.04 +/- 0.45 vs 0.76 +/- 0.25 mumol/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.</p>
dc.identifier.submissionpathoapubs/166
dc.contributor.departmentDepartment of Medicine, Division of Pulmonary, Allergy & Critical Care
dc.contributor.departmentDepartment of Surgery
dc.contributor.departmentDepartment of Anesthesiology
dc.source.pages353-7


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