| pubmed-article:6866727 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6866727 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:6866727 | lifeskim:mentions | umls-concept:C1159441 | lld:lifeskim |
| pubmed-article:6866727 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:6866727 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:6866727 | pubmed:dateCreated | 1983-8-11 | lld:pubmed |
| pubmed-article:6866727 | pubmed:abstractText | The role of endothelial cells in the dilatory response of arteries to hypoxia was studied in vitro using perfused arterial segments of rat and dog. The pO2 of the intra- and extraluminal perfusate could be varied separately. Intraluminal hypoxia (pO2 of 40 mmHg) induced a dilation irrespective of extraluminal pO2 level. On the contrary extraluminal hypoxia could not elicit a dilation during intraluminal normoxic perfusion. Dilation during extraluminal hypoxia could only be induced if the segment was not intraluminally perfused. The dilatory response to intraluminal hypoxia was abolished after enzymatical or mechanical removal of the endothelium. While theophylline and lipoxygenase inhibitors did not influence this endothelium-induced dilation, a significant reduction of the response could be observed after incubation with indomethacin. These results support the concept that prostacyclin (PGI2) might be involved in the hypoxic endothelium-induced dilation. | lld:pubmed |
| pubmed-article:6866727 | pubmed:language | eng | lld:pubmed |
| pubmed-article:6866727 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6866727 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:6866727 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6866727 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6866727 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6866727 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:6866727 | pubmed:issn | 0031-6768 | lld:pubmed |
| pubmed-article:6866727 | pubmed:author | pubmed-author:BusseRR | lld:pubmed |
| pubmed-article:6866727 | pubmed:author | pubmed-author:PohlUU | lld:pubmed |
| pubmed-article:6866727 | pubmed:author | pubmed-author:KellnerCC | lld:pubmed |
| pubmed-article:6866727 | pubmed:author | pubmed-author:KlemmUU | lld:pubmed |
| pubmed-article:6866727 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6866727 | pubmed:volume | 397 | lld:pubmed |
| pubmed-article:6866727 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6866727 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6866727 | pubmed:pagination | 78-80 | lld:pubmed |
| pubmed-article:6866727 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:6866727 | pubmed:meshHeading | pubmed-meshheading:6866727-... | lld:pubmed |
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| pubmed-article:6866727 | pubmed:meshHeading | pubmed-meshheading:6866727-... | lld:pubmed |
| pubmed-article:6866727 | pubmed:meshHeading | pubmed-meshheading:6866727-... | lld:pubmed |
| pubmed-article:6866727 | pubmed:meshHeading | pubmed-meshheading:6866727-... | lld:pubmed |
| pubmed-article:6866727 | pubmed:meshHeading | pubmed-meshheading:6866727-... | lld:pubmed |
| pubmed-article:6866727 | pubmed:meshHeading | pubmed-meshheading:6866727-... | lld:pubmed |
| pubmed-article:6866727 | pubmed:meshHeading | pubmed-meshheading:6866727-... | lld:pubmed |
| pubmed-article:6866727 | pubmed:year | 1983 | lld:pubmed |
| pubmed-article:6866727 | pubmed:articleTitle | Endothelial cells are involved in the vasodilatory response to hypoxia. | lld:pubmed |
| pubmed-article:6866727 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6866727 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:6866727 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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