Inhaled carbon monoxide protects time-dependently from loss of hypoxic pulmonary vasoconstriction in endotoxemic mice
| Autor: | Nora, Jahn, Regis R, Lamberts, Cornelius J, Busch, Maria T, Voelker, Thilo, Busch, Marleen J A, Koel-Simmelink, Charlotte E, Teunissen, Daniel D, Oswald, Stephan A, Loer, Udo X, Kaisers, Jörg, Weimann |
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| Rok vydání: | 2015 |
| Předmět: |
Lipopolysaccharides
Male Carbon Monoxide HPV Time Factors Research Membrane Proteins Nitric Oxide Synthase Type II Pulmonary Artery Endotoxemia Drug Administration Schedule Mice Inbred C57BL CO Disease Models Animal Vasoconstriction Sepsis Administration Inhalation Pulmonary circulation Cytokines Animals Arterial Pressure RNA Messenger Inflammation Mediators Hypoxia Heme Oxygenase-1 |
| Zdroj: | Respiratory Research |
| ISSN: | 1465-993X |
| Popis: | Background Inhaled carbon monoxide (CO) appears to have beneficial effects on endotoxemia-induced impairment of hypoxic pulmonary vasoconstriction (HPV). This study aims to specify correct timing of CO application, it’s biochemical mechanisms and effects on inflammatory reactions. Methods Mice (C57BL/6; n = 86) received lipopolysaccharide (LPS, 30 mg/kg) intraperitoneally and subsequently breathed 50 ppm CO continuously during defined intervals of 3, 6, 12 or 18 h. Two control groups received saline intraperitoneally and additionally either air or CO, and one control group received LPS but breathed air only. In an isolated lung perfusion model vasoconstrictor response to hypoxia (FiO2 = 0.01) was quantified by measurements of pulmonary artery pressure. Pulmonary capillary pressure was estimated by double occlusion technique. Further, inflammatory plasma cytokines and lung tissue mRNA of nitric-oxide-synthase-2 (NOS-2) and heme oxygenase-1 (HO-1) were measured. Results HPV was impaired after LPS-challenge (p |
| Databáze: | OpenAIRE |
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