| http://purl.uniprot.org/citations/1860178 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/1860178 | http://www.w3.org/2000/01/rdf-schema#comment | "Pathophysiological roles of endogenous endothelin have been studied from the viewpoint of its contribution to the extension of myocardial infarct size. A monoclonal antibody against endothelin 1 (AwETN40) suppressed changes induced by endothelin 1 and endothelin 2 but did not modify those by endothelin 3 in vivo or in vitro. Effects of AwETN40 on myocardial infarct size were investigated. Coronary ligation (1 hour) and reperfusion (24 hours) in rats caused infarction in 35% of the left ventricle. Repetitive or single administration of AwETN40 reduced the infarct size; an intravenous injection of 22.5 mg/kg of the antibody 5 minutes after coronary occlusion or 5 minutes before reperfusion reduced the size by 38% or 31% of the control, respectively. Plasma and tissue endothelin 1 and plasma big endothelin 1 in rats were measured at various stages after occlusion. Plasma endothelin 1 showed a fourfold increase 10 minutes after reperfusion (from 1.02 to 3.96 pg/ml) and had returned to the control value after 8 hours. Plasma big endothelin 1 showed changes similar to those of plasma endothelin 1. No significant changes in plasma endothelin 2 and endothelin 3 were observed. Cardiac tissue contained seven times as much endothelin 1 as the control value 1 hour after reperfusion (4.59 versus 33.1 pg/g tissue), and a high concentration (13.2 pg/g tissue) was maintained even after 48 hours. We concluded that an increase in endogenous endothelin 1 plays an important role in the extension of myocardial infarct size."xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.org/dc/terms/identifier | "doi:10.1161/01.res.69.2.370"xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/author | "Fujino M."xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/author | "Watanabe T."xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/author | "Suzuki N."xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/author | "Shimamoto N."xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/author | "Imada A."xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/date | "1991"xsd:gYear |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/name | "Circ Res"xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/pages | "370-377"xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/title | "Contribution of endogenous endothelin to the extension of myocardial infarct size in rats."xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://purl.uniprot.org/core/volume | "69"xsd:string |
| http://purl.uniprot.org/citations/1860178 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/1860178 |
| http://purl.uniprot.org/citations/1860178 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/1860178 |
| http://purl.uniprot.org/uniprot/P23943#attribution-18574F96056B8129C9F1C8878F038773 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/1860178 |
| http://purl.uniprot.org/uniprot/#_G3V771-mappedCitation-1860178 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/1860178 |
| http://purl.uniprot.org/uniprot/#_P23943-mappedCitation-1860178 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/1860178 |
| http://purl.uniprot.org/uniprot/P23943 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/1860178 |
| http://purl.uniprot.org/uniprot/G3V771 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/1860178 |