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Rothoerl, Ralf Dirk ; Schebesch, Karl-Michael ; Kubitza, Marion ; Woertgen, Chris ; Brawanski, Alexander ; Pina, Ana-Luisa

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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Details

DokumentenartArtikel
Titel eines Journals oder einer ZeitschriftCerebrovascular diseases (Basel, Switzerland)
Verlag:KARGER
Ort der Veröffentlichung:BASEL
Band:22
Nummer des Zeitschriftenheftes oder des Kapitels:2-3
Seitenbereich:S. 143-149
Datum2006
InstitutionenMedizin > Lehrstuhl für Neurochirurgie
Identifikationsnummer
WertTyp
16691023PubMed-ID
10.1159/000093243DOI
Stichwörter / KeywordsINTERCELLULAR-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-Klassifikation600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin
StatusVeröffentlicht
BegutachtetJa, diese Version wurde begutachtet
An der Universität Regensburg entstandenJa
Dokumenten-ID1235

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