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Cerebral arterial wall remodeling following subarachnoid hemorrhage (853.5)
Author(s) -
Lachkar Nadia,
Guvenc Tuna Bilge,
Bakker Erik,
Vos Judith,
VanBavel Ed
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.853.5
Subject(s) - subarachnoid hemorrhage , medicine , vasospasm , myograph , vasoconstriction , cerebral arteries , basilar artery , ischemia , cardiology , cerebral vasospasm , artery
Delayed cerebral ischemia (DCI) is a serious complication after aneurysmal subarachnoid hemorrhage (SAH). A significant cause of DCI is vasospasm of the major cerebral arteries. We hypothesized that vasospasm is not simply vasoconstriction but an ongoing process of remodeling of the vascular wall, and tissue transglutaminase 2 (TG2) may be involved in the remodeling of cerebral arteries after SAH. The exposure to subarachnoid blood was mimicked in an in vitro wire myograph study on rat middle cerebral arteries (MCA) and basilar arteries. Smooth muscle cell (SMC) contractile plasticity and matrix remodeling were assessed from changes in wall tension during full activation and total relaxation. 16 hours of incubation with blood caused contractile activation of SMCs, and induced luminal narrowing and inward matrix remodeling of both the MCA and basilar artery. Incubation with TG2 inhibitor L682.777 countered the effect of blood induced remodeling. In an in vivo prechiasmatic injection model for SAH performed in mice (2 days) and rats (3 days), we found no SMC plasticity and no vascular wall remodeling, despite early changes in cerebral blood flow. Our in vitro data suggest that exposure of the cerebral arteries with blood results in vascular wall remodeling and luminal narrowing in a TG2‐dependent manner. However, in the in vivo SAH models such changes were not observed. Grant Funding Source : Supported by SMART FP7 Marie Curie ITN number 235711