Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-9-14
pubmed:abstractText
Because carbon monoxide (CO) has been proposed to have anti-inflammatory properties, we sought protective effects of CO in pulmonary O(2) toxicity, which leads rapidly to lung inflammation and respiratory failure. Based on published studies, we hypothesized that CO protects the lung against O(2) by selectively increasing expression of antioxidant enzymes, thereby decreasing oxidative injury and inflammation. Rats exposed to O(2) with or without CO [50-500 parts/million (ppm)] for 60 h were compared for lung wet-to-dry weight ratio (W/D), pleural fluid volume, myeloperoxidase (MPO) activity, histology, expression of heme oxygenase-1 (HO-1), and manganese superoxide dismutase (Mn SOD) proteins. The brains were evaluated for histological evidence of damage from CO. In O(2)-exposed animals, lung W/D increased from 4.8 in normal rats to 6.3; however, only CO at 200 and 500 ppm decreased W/D significantly (to 5.9) during O(2) exposure. Large volumes of pleural fluid accumulated in all rats, with no significant CO treatment effect. Lung MPO values increased after O(2) and were not attenuated by CO treatment. CO did not enhance lung expression of oxidant-responsive proteins Mn SOD and HO-1. Animals receiving O(2) and CO at 200 or 500 ppm showed significant apoptotic cell death in the cortex and hippocampus by immunochemical staining. Thus significant protection by CO against O(2)-induced lung injury could not be confirmed in rats, even at CO concentrations associated with apoptosis in the brain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1040-0605
pubmed:author
pubmed:issnType
Print
pubmed:volume
281
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
L949-57
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed-meshheading:11557599-Animals, pubmed-meshheading:11557599-Blood Gas Analysis, pubmed-meshheading:11557599-Blotting, Western, pubmed-meshheading:11557599-Brain Diseases, pubmed-meshheading:11557599-Carbon Monoxide, pubmed-meshheading:11557599-Carboxyhemoglobin, pubmed-meshheading:11557599-Heme Oxygenase (Decyclizing), pubmed-meshheading:11557599-Heme Oxygenase-1, pubmed-meshheading:11557599-Hyperoxia, pubmed-meshheading:11557599-Lung, pubmed-meshheading:11557599-Male, pubmed-meshheading:11557599-Oxidative Stress, pubmed-meshheading:11557599-Oxygen, pubmed-meshheading:11557599-Pleural Effusion, pubmed-meshheading:11557599-Pneumonia, pubmed-meshheading:11557599-Pulmonary Edema, pubmed-meshheading:11557599-Rats, pubmed-meshheading:11557599-Rats, Sprague-Dawley, pubmed-meshheading:11557599-Superoxide Dismutase
pubmed:year
2001
pubmed:articleTitle
Inhaled carbon monoxide and hyperoxic lung injury in rats.
pubmed:affiliation
Division of Pulmonary Medicine, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
pubmed:publicationType
Journal Article