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Endothelial injury and inflammatory response induced by hemodynamic changes preceding intracranial aneurysm formation: experimental study in rats.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Jamous, Mohammad A. Nagahiro, Shinji Kitazato, Keiko T. Tamura, Tetsuya Aziz, Hani Abdel Shono, Masayuki Satoh, Koichi |
| Copyright Year | 2007 |
| Abstract | OBJECT 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. METHODS The authors induced cerebral aneurysms by renal hypertension and right common carotid artery ligation in 40 male Sprague-Dawley rats; 10 intact rats served as the controls. The anterior cerebral artery-olfactory artery bifurcation was assessed morphologically by using vascular corrosion casts of Batson plastic reagent and immunohistochemically by using antibodies against endothelial nitric oxide synthase, alpha-smooth muscle actin, macrophages, and matrix metalloproteinase-9. RESULTS 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). CONCLUSIONS 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. |
| Starting Page | 16 |
| Ending Page | 24 |
| Page Count | 9 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://thejns.org/downloadpdf/journals/j-neurosurg/107/2/article-p405.pdf |
| PubMed reference number | 17695397v1 |
| Volume Number | 107 |
| Issue Number | 2 |
| Journal | Journal of neurosurgery |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Carotid Arteries Cascade Device Component Cerebral Aneurysm Corrosion Endothelium Hemodynamics Hypertensive disease Intracranial Aneurysm Ligation Morbidity - disease rate Nitric Oxide Synthase Reagents Renal hypertension Right common carotid artery structure Rupture Smooth muscle (tissue) Structure of anterior cerebral artery Structure of cerebral artery Subarachnoid Hemorrhage Wounds and Injuries inflammatory response stage II childhood Hodgkin's lymphoma |
| Content Type | Text |
| Resource Type | Article |
