pubmed-article:7701873 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7701873 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:7701873 | lifeskim:mentions | umls-concept:C0079284 | lld:lifeskim |
pubmed-article:7701873 | lifeskim:mentions | umls-concept:C0034735 | lld:lifeskim |
pubmed-article:7701873 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
pubmed-article:7701873 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:7701873 | pubmed:dateCreated | 1995-4-28 | lld:pubmed |
pubmed-article:7701873 | pubmed:abstractText | Plasma endothelin response to a standardized cold challenge in 7 patients with primary Raynaud's phenomenon and 7 controls using a sensitive radioimmunoassay was measured. There was no difference between resting levels of plasma endothelin in patients with primary Raynaud's phenomenon (2.6 fmol/ml) and controls (2.4 fmol/ml). A decrease in plasma endothelin levels in both groups of patients during the initial phase of the cold challenge was detected; this was more pronounced in the patients with Raynaud's phenomenon. These results suggest that there is no persistent stimulus to overproduction of endothelin. The fall in levels in patients with Raynaud's phenomenon during the initial phase of the cold challenge might suggest that a different vasoconstrictive factor is initiating the start of the vasospastic process, with the decreased endothelin levels being a reactive response to increased vasoconstriction produced by this alternative factor. | lld:pubmed |
pubmed-article:7701873 | pubmed:language | eng | lld:pubmed |
pubmed-article:7701873 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7701873 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:7701873 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7701873 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7701873 | pubmed:month | Nov | lld:pubmed |
pubmed-article:7701873 | pubmed:issn | 0001-5555 | lld:pubmed |
pubmed-article:7701873 | pubmed:author | pubmed-author:BottomleyWW | lld:pubmed |
pubmed-article:7701873 | pubmed:author | pubmed-author:GoodfieldMM | lld:pubmed |
pubmed-article:7701873 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7701873 | pubmed:volume | 74 | lld:pubmed |
pubmed-article:7701873 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7701873 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7701873 | pubmed:pagination | 433-4 | lld:pubmed |
pubmed-article:7701873 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
pubmed-article:7701873 | pubmed:meshHeading | pubmed-meshheading:7701873-... | lld:pubmed |
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pubmed-article:7701873 | pubmed:meshHeading | pubmed-meshheading:7701873-... | lld:pubmed |
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pubmed-article:7701873 | pubmed:meshHeading | pubmed-meshheading:7701873-... | lld:pubmed |
pubmed-article:7701873 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7701873 | pubmed:articleTitle | A pathogenic role for endothelin in Raynaud's phenomenon? | lld:pubmed |
pubmed-article:7701873 | pubmed:affiliation | Department of Dermatology, Leeds General Infirmary, UK. | lld:pubmed |
pubmed-article:7701873 | pubmed:publicationType | Journal Article | lld:pubmed |