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ICAM-1 and VCAM-1 expression following aneurysmal subarachnoid hemorrhage and their possible role in the pathophysiology of subsequent ischemic deficits
Rothoerl, Ralf Dirk, Schebesch, Karl-Michael, Kubitza, Marion, Woertgen, Chris, Brawanski, Alexander und Pina, Ana-Luisa (2006) ICAM-1 and VCAM-1 expression following aneurysmal subarachnoid hemorrhage and their possible role in the pathophysiology of subsequent ischemic deficits. Cerebrovascular diseases (Basel, Switzerland) 22 (2-3), S. 143-149.Veröffentlichungsdatum dieses Volltextes: 05 Aug 2009 13:26
Artikel
DOI zum Zitieren dieses Dokuments: 10.5283/epub.1235
Zusammenfassung
Background: The pathophysiology of ischemic cerebral lesions following aneurysmal subarachnoid hemorrhage ( SAH) is poorly understood. There is growing evidence that inflammatory reactions could be involved in the pathogenesis of such delayed occurring ischemic lesions. The aim of this study was to evaluate adhesion molecules with regard to these lesions following SAH. Methods: Serum and ...
Background: The pathophysiology of ischemic cerebral lesions following aneurysmal subarachnoid hemorrhage ( SAH) is poorly understood. There is growing evidence that inflammatory reactions could be involved in the pathogenesis of such delayed occurring ischemic lesions. The aim of this study was to evaluate adhesion molecules with regard to these lesions following SAH. Methods: Serum and cerebrospinal fluid ( CSF) samples were taken daily from 15 patients up to day 9 after SAH and evaluated for intercellular adhesion molecule-1 ( ICAM-1) and vascular adhesion molecule- 1 ( VCAM- 1). Results: CSF and serum samples correlated well during nearly the whole time course ( p < 0.0001). A secondary increase in ICAM-1 and VCAM- 1 in the serum and CSF correlated with an increase in flow velocity in the transcranial Doppler ( p > 0.0001 and p < 0.007) but not to a delayed lesion in the CT scan. Conclusion: We believe that inflammatory processes are involved in the pathogenesis of cerebral vasospasm but they might only be a part of a multifactorial pathogenesis. Copyright (c) 2006 S. Karger AG, Basel
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| Dokumentenart | Artikel | ||||||
| Titel eines Journals oder einer Zeitschrift | Cerebrovascular diseases (Basel, Switzerland) | ||||||
| Verlag: | KARGER | ||||||
|---|---|---|---|---|---|---|---|
| Ort der Veröffentlichung: | BASEL | ||||||
| Band: | 22 | ||||||
| Nummer des Zeitschriftenheftes oder des Kapitels: | 2-3 | ||||||
| Seitenbereich: | S. 143-149 | ||||||
| Datum | 2006 | ||||||
| Institutionen | Medizin > Lehrstuhl für Neurochirurgie | ||||||
| Identifikationsnummer |
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| Stichwörter / Keywords | INTERCELLULAR-ADHESION MOLECULE-1; CEREBRAL VASOSPASM; CULTURED ENDOTHELIUM; GRANULOCYTE ADHESION; MONOCLONAL-ANTIBODY; CEREBROSPINAL-FLUID; ARTERIAL-WALL; E-SELECTIN; RATS; INFLAMMATION; adhesion molecules; intercellular adhesion molecule-1; vascular cell adhesion molecule-1; subarachnoid hemorrhage; vasospasm; ischemic neurological deficit, delayed | ||||||
| Dewey-Dezimal-Klassifikation | 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin | ||||||
| Status | Veröffentlicht | ||||||
| Begutachtet | Ja, diese Version wurde begutachtet | ||||||
| An der Universität Regensburg entstanden | Ja | ||||||
| Dokumenten-ID | 1235 |
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