{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T08:45:12Z","timestamp":1790757912746,"version":"4.1.0"},"reference-count":25,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNS"],"published-print":{"date-parts":[[2007,8]]},"abstract":"<jats:sec>\n<jats:title>Object<\/jats:title>\n<jats:p>Intracranial aneurysms are the leading cause of subarachnoid hemorrhage, which is associated with high morbidity and mortality rates. Despite advances in the microsurgical and endovascular treatment of intracranial aneurysms, little is known about the mechanisms by which they originate, grow, and rupture. To clarify the series of early events leading to formation of intracranial aneurysms, the authors compared aneurysmal morphological changes on vascular corrosion casts with parallel pathological changes in the cerebral arteries of rats.<\/jats:p><\/jats:sec>\n<jats:sec>\n<jats:title>Methods<\/jats:title>\n<jats:p>The authors induced cerebral aneurysms by renal hypertension and right common carotid artery ligation in 40 male Sprague\u2013Dawley rats; 10 intact rats served as the controls. The anterior cerebral artery\u2013olfactory artery bifurcation was assessed morphologically by using vascular corrosion casts of Batson plastic reagent and immunohis-tochemically by using antibodies against endothelial nitric oxide synthase, \u03b1\u2013smooth muscle actin, macrophages, and matrix metalloproteinase\u20139.<\/jats:p><\/jats:sec>\n<jats:sec>\n<jats:title>Results<\/jats:title>\n<jats:p>Surgically treated rats manifested different degrees of aneurysmal changes. Based on these staged changes, the authors propose that the formation of intracranial aneurysms starts with endothelial injury at the apical intimal pad (Stage I); this leads to the formation of an inflammatory zone (Stage II), followed by a partial tear or defect in the inflammatory zone. Expansion of this defect forms the nidus of the intracranial aneurysm (Stage III).<\/jats:p><\/jats:sec>\n<jats:sec>\n<jats:title>Conclusions<\/jats:title>\n<jats:p>This is the first study to demonstrate the in vivo mechanisms of intracranial aneurysm formation. The inflammatory response that follows endothelial injury is the basic step in the pathogenesis of these lesions. In this study the investigators have expanded the understanding of the origin of intracranial aneurysms and have contributed to the further development of measures to prevent and treat aneurysms.<\/jats:p><\/jats:sec>","DOI":"10.3171\/jns-07\/08\/0405","type":"journal-article","created":{"date-parts":[[2008,1,24]],"date-time":"2008-01-24T12:50:52Z","timestamp":1201179052000},"page":"405-411","source":"Crossref","is-referenced-by-count":121,"title":["Endothelial injury and inflammatory response induced by hemodynamic changes preceding intracranial aneurysm formation: experimental study in rats"],"prefix":"10.3171","volume":"107","author":[{"given":"Mohammad A.","family":"Jamous","sequence":"first","affiliation":[{"name":"Department of Neurosciences, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan"},{"name":"Department of Neurosurgery,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinji","family":"Nagahiro","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keiko T.","family":"Kitazato","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tetsuya","family":"Tamura","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hani Abdel","family":"Aziz","sequence":"additional","affiliation":[{"name":"Department of Neurosciences, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masayuki","family":"Shono","sequence":"additional","affiliation":[{"name":"Support Center for Advanced Medical Sciences, The Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koichi","family":"Satoh","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"key":"b1-1070405","series-title":"Stroke","doi-asserted-by":"publisher","first-page":"1342","DOI":"10.1161\/01.STR.25.7.1342","article-title":"Initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage","volume":"25","author":"Broderick","year":"1994"},{"key":"b2-1070405","series-title":"Neurosurgery","doi-asserted-by":"publisher","first-page":"1137","DOI":"10.1097\/00006123-199911000-00024","article-title":"Inflammation and intracranial aneurysms","volume":"45","author":"Chyatte","year":"1999"},{"key":"b3-1070405","series-title":"J Clin Invest","doi-asserted-by":"publisher","first-page":"1116","DOI":"10.1172\/JCI115929","article-title":"Nitric oxide, an endothelial cell relaxation factor, inhibits neutrophil super-oxide anion production via a direct action on the NADPH oxidase","volume":"90","author":"Clancy","year":"1992"},{"key":"b4-1070405","series-title":"J Clin Invest","doi-asserted-by":"publisher","first-page":"1121","DOI":"10.1172\/JCI111298","article-title":"Influence of hemodynamic forces on vascular endothelial function. 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