| pubmed-article:18455212 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18455212 | lifeskim:mentions | umls-concept:C0332157 | lld:lifeskim |
| pubmed-article:18455212 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:18455212 | lifeskim:mentions | umls-concept:C0012151 | lld:lifeskim |
| pubmed-article:18455212 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:18455212 | pubmed:dateCreated | 2008-7-15 | lld:pubmed |
| pubmed-article:18455212 | pubmed:abstractText | Environmental air pollution is associated with adverse cardiovascular events, including increased hospital admissions due to heart failure and myocardial infarction. The exact mechanism(s) by which air pollution affects the heart and vasculature is currently unknown. Recent studies have found that exposure to air pollution enhances arterial vasoconstriction in humans and animal models. Work in our laboratory has shown that diesel emissions (DE) enhance vasoconstriction of mouse coronary arteries. Thus, we hypothesized that DE could enhance vasoconstriction in arteries and veins through uncoupling of endothelial nitric oxide synthase (eNOS). To test this hypothesis, we first bubbled DE through a physiological saline solution and exposed isolated mesenteric veins. Second, we exposed animals, whole body, to DE at 350 microg/m(3) for 4 h, after which mesenteric arteries and veins were isolated. Results from these experiments show that saline bubbled with DE as well as inhaled DE enhances vasoconstriction in veins but not arteries. Exposure to several representative volatile organic compounds found in the DE-exposed saline did not enhance arterial constriction. L-nitro-arginine-methyl-ester (L-NAME), an eNOS inhibitor, normalized the control vessels to the DE-exposed vessels implicating an uncoupling of eNOS as a mechanism for enhanced vasoconstriction. The principal conclusions of this research are 1) veins exhibit endothelial dysfunction following in vivo and ex vivo exposures to DE, 2) veins appear to be more sensitive to DE effects than arteries, and 3) DE components most likely induce endothelial dysfunction through the uncoupling of eNOS. | lld:pubmed |
| pubmed-article:18455212 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18455212 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18455212 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18455212 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18455212 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18455212 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18455212 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18455212 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18455212 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:18455212 | pubmed:issn | 0041-008X | lld:pubmed |
| pubmed-article:18455212 | pubmed:author | pubmed-author:CampenMatthew... | lld:pubmed |
| pubmed-article:18455212 | pubmed:author | pubmed-author:LundAmie KAK | lld:pubmed |
| pubmed-article:18455212 | pubmed:author | pubmed-author:KnucklesTravi... | lld:pubmed |
| pubmed-article:18455212 | pubmed:author | pubmed-author:LucasSelita... | lld:pubmed |
| pubmed-article:18455212 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18455212 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:18455212 | pubmed:volume | 230 | lld:pubmed |
| pubmed-article:18455212 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18455212 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18455212 | pubmed:pagination | 346-51 | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:meshHeading | pubmed-meshheading:18455212... | lld:pubmed |
| pubmed-article:18455212 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18455212 | pubmed:articleTitle | Diesel exhaust exposure enhances venoconstriction via uncoupling of eNOS. | lld:pubmed |
| pubmed-article:18455212 | pubmed:affiliation | Toxicology Division, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA. | lld:pubmed |
| pubmed-article:18455212 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18455212 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18455212 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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