{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T14:34:33Z","timestamp":1773758073746,"version":"3.50.1"},"reference-count":0,"publisher":"Hogrefe Publishing Group","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Vasa"],"published-print":{"date-parts":[[2000,8,1]]},"abstract":"<jats:p> Background: It has been postulated that adhesion molecules (AM) may be involved in development and progression of human atherosclerosis. We examined whether prostaglandin (PG) E1 affects circulating levels of the AM (ICAM-1, VCAM-1 and E-selectin) in peripheral vascular disease (PVD) patients. Methods and results: AM are significantly (p &lt; 0.01) increased in PVD (n = 65) as compared to controls (n = 31). There was no influence of risk factors. 26 PVD-patients received 2 different schemes of PGE1-therapy (group A [n = 17]; 5 ng PGE1\/kg\/min \u00d7 6 h \u00d7 5 d \u00d7 4 wk; group B [n = 9]; 60 mug PGE1\/2 h \u00d7 5 d \u00d7 2 wk). PGE1 decreases all the AM significantly (p &lt; 0.01) using both therapeutic schemes. Stopping PGE1-therapy reverses values within about 4 weeks. Details on therapeutic regimens (dose, duration, route, etc.) and individual response still need to be assessed. Conclusion: Our results indicate that PGE1-treatment of PVD is associated with a significant benefit on circulating AM. These findings are in line with the described anti-inflammatory actions of PGE1 and may represent a further contributing factor to the great variety of beneficial actions of PGE1 on human atherosclerosis. <\/jats:p>","DOI":"10.1024\/0301-1526.29.3.179","type":"journal-article","created":{"date-parts":[[2006,1,31]],"date-time":"2006-01-31T12:25:19Z","timestamp":1138710319000},"page":"179-185","source":"Crossref","is-referenced-by-count":13,"title":["Prostaglandin E1-Therapie vermindert zirkulierende Adh\u00e4sionsmolek\u00fcle (ICAM, E-Selectin, VCAM-1) bei Patienten mit peripherer arterieller Verschlusskrankheit"],"prefix":"10.1024","volume":"29","author":[{"family":"Palumbo","sequence":"first","affiliation":[{"name":"Institute of Nuclear Medicine, University of Perugia, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"family":"Oguogho","sequence":"additional","affiliation":[{"name":"Department of Nuclear Medicine, University of Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"family":"Fitscha","sequence":"additional","affiliation":[{"name":"Wilhelm Auerswald-Atherosclerosis Research Group (ASF) Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Helmut","family":"Sinzinger","sequence":"additional","affiliation":[{"name":"Department of Nuclear Medicine, University of Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"101","container-title":["Vasa"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/econtent.hogrefe.com\/doi\/pdf\/10.1024\/0301-1526.29.3.179","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,8]],"date-time":"2022-05-08T11:04:07Z","timestamp":1652007847000},"score":1,"resource":{"primary":{"URL":"https:\/\/econtent.hogrefe.com\/doi\/10.1024\/0301-1526.29.3.179"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2000,8,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2000,8,1]]}},"alternative-id":["10.1024\/0301-1526.29.3.179"],"URL":"https:\/\/doi.org\/10.1024\/0301-1526.29.3.179","relation":{},"ISSN":["0301-1526","1664-2872"],"issn-type":[{"value":"0301-1526","type":"print"},{"value":"1664-2872","type":"electronic"}],"subject":[],"published":{"date-parts":[[2000,8,1]]}}}