{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T12:32:53Z","timestamp":1772109173876,"version":"3.50.1"},"reference-count":35,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2001,5,1]],"date-time":"2001-05-01T00:00:00Z","timestamp":988675200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Lipids"],"published-print":{"date-parts":[[2001,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The importance of low\u2010density lipoprotein (LDL) in the etiology of atherosclerosis is well recognized. We have established a reproducible stenosis model in hypercholesterolemic hamsters, and the process of arterial stenosis by thrombus or neointima was studied and compared with that in normal hamsters. The level of plasma LDL was 4.6 times higher in hamsters fed a high\u2010cholesterol diet than in hamsters fed normal food. Endothelial injury in right common carotid arteries was induced using a modified catheter. Arterial blood flow was monitored continuously using a Doppler flow probe. Arterial patency after the initiation of injury in high\u2010cholesterol hamsters was significantly changed as compared with that of normal hamsters. Neointima was observed 2 wk after the vascular injury. The neointimal area of high\u2010cholesterol hamsters was significantly larger than that of normal hamsters. To characterize the stenosis in hypercholesterolemic hamsters, we measured platelet aggregation, thrombin time, activated partial thromboplastin time, and proliferating smooth muscle cells (SMC) <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic>. The half\u2010maximal inhibitory concentration value for platelet aggregation induced by thrombin or collagen, the DNA synthesis stimulated by plateletderived growth factor (PDGF)\u2010BB, and 5\u2010bromo\u20102\u2010deoxy\u2010uridine labeling indices (proliferating index of SMC <jats:italic>in vivo<\/jats:italic>) in high\u2010cholesterol hamsters were each significantly higher than the comparable value from normal hamsters. However, specific binding of PDGF\u2010BB in SMC was not different between the two types of hamsters. Furthermore, we investigated the inhibitory effects of probucol or losartan on neointima formation using this model. Probucol, but not losartan, significantly reduced the neointimal area in hypercholesterolemic hamsters. These findings indicated that high levels of plasma LDL strongly contributed to the development of thrombus and neointima formation <jats:italic>via<\/jats:italic> both up\u2010regulation of platelet aggregation and the enhancement of SMC proliferation. This stenosis model may be useful for the investigation of hypercholesterolemia\u2010associated cardiovascular diseases.<\/jats:p>","DOI":"10.1007\/s11745-001-0742-4","type":"journal-article","created":{"date-parts":[[2006,11,15]],"date-time":"2006-11-15T20:22:06Z","timestamp":1163622126000},"page":"453-460","source":"Crossref","is-referenced-by-count":4,"title":["Characterization of simple and reproducible vascular stenosis model in hypercholesterolemic hamsters"],"prefix":"10.1002","volume":"36","author":[{"given":"Hiroyuki","family":"Matsuno","sequence":"first","affiliation":[{"name":"Department of Pharmacology Gifu University School of Medicine Tsukasa\u2010machi 40 Gifu 500 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Osamu","family":"Kozawa","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Gifu University School of Medicine Tsukasa\u2010machi 40 Gifu 500 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