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Subarachnoid hemorrhage induces upregulation of vascular receptors and reduction in rCBF via an ERKI/2 mechanism

Ansar, Saema LU ; Lundager Hansen, Jakob LU and Edvinsson, Lars LU (2008) 9th International Conference on Cerebral Vasospasm 104. p.65-67
Abstract
Previous studies have shown that endothelin type B (ETB) and 5-hydroxytryptamine type IB (5-HTIB) receptors are upregulated following subarachnoid hemorrhage (SAH). The purpose of the present study was to test whether extracellular signal-regulated kinase (ERKI/2) inhibition could alter the degree of SAH induced receptor upregulation in addition to prevent the cerebral blood flow (CBF) reduction. The ERKI/2 inhibitor SB386023-b was injected intra cisternally in conjunction with and after the induced SAH in rats. Two days after SAH cerebral arteries were harvested and the contractile response to endothelin-1 (ET-I) and 5-carboxamidotryptamine (5-CT) were investigated with a myograph. The contractile responses to ET-I and 5-CT were increased... (More)
Previous studies have shown that endothelin type B (ETB) and 5-hydroxytryptamine type IB (5-HTIB) receptors are upregulated following subarachnoid hemorrhage (SAH). The purpose of the present study was to test whether extracellular signal-regulated kinase (ERKI/2) inhibition could alter the degree of SAH induced receptor upregulation in addition to prevent the cerebral blood flow (CBF) reduction. The ERKI/2 inhibitor SB386023-b was injected intra cisternally in conjunction with and after the induced SAH in rats. Two days after SAH cerebral arteries were harvested and the contractile response to endothelin-1 (ET-I) and 5-carboxamidotryptamine (5-CT) were investigated with a myograph. The contractile responses to ET-I and 5-CT were increased after SAH compared to sham. Administration of SB-386023-b prevented the upregulated contraction elicited by application of ET-I and 5-CT in cerebral arteries. Regional CBF evaluated by an autoradiographic technique, revealed a reduced CBF by 50% after SAH this was prevented by treatment with SB-386023-b. The results indicate that an ERKI/2 mechanism is involved in cerebral vasospasm and ischemia associated with SAH. (Less)
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author
; and
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
keywords
signal-regulated kinase (ERKI/2), extracellular, cerebral blood flow (CBF), cerebral ischemia, subarachnoid hemorrhage (SAH)
host publication
Cerebral Vasospasm: New Strategies in Research and Treatment
volume
104
pages
65 - 67
publisher
Springer
conference name
9th International Conference on Cerebral Vasospasm
conference location
Istanbul, Turkey
conference dates
2006-06-27 - 2006-06-30
external identifiers
  • wos:000256013000012
  • scopus:77957559398
ISSN
0065-1419
ISBN
978-3-211-75717-8
DOI
10.1007/978-3-211-75718-5_12
language
English
LU publication?
yes
id
8e49a584-439e-427b-b550-edb5339c914c (old id 1407181)
date added to LUP
2016-04-01 13:53:39
date last changed
2024-10-10 09:16:31
@inproceedings{8e49a584-439e-427b-b550-edb5339c914c,
  abstract     = {{Previous studies have shown that endothelin type B (ETB) and 5-hydroxytryptamine type IB (5-HTIB) receptors are upregulated following subarachnoid hemorrhage (SAH). The purpose of the present study was to test whether extracellular signal-regulated kinase (ERKI/2) inhibition could alter the degree of SAH induced receptor upregulation in addition to prevent the cerebral blood flow (CBF) reduction. The ERKI/2 inhibitor SB386023-b was injected intra cisternally in conjunction with and after the induced SAH in rats. Two days after SAH cerebral arteries were harvested and the contractile response to endothelin-1 (ET-I) and 5-carboxamidotryptamine (5-CT) were investigated with a myograph. The contractile responses to ET-I and 5-CT were increased after SAH compared to sham. Administration of SB-386023-b prevented the upregulated contraction elicited by application of ET-I and 5-CT in cerebral arteries. Regional CBF evaluated by an autoradiographic technique, revealed a reduced CBF by 50% after SAH this was prevented by treatment with SB-386023-b. The results indicate that an ERKI/2 mechanism is involved in cerebral vasospasm and ischemia associated with SAH.}},
  author       = {{Ansar, Saema and Lundager Hansen, Jakob and Edvinsson, Lars}},
  booktitle    = {{Cerebral Vasospasm: New Strategies in Research and Treatment}},
  isbn         = {{978-3-211-75717-8}},
  issn         = {{0065-1419}},
  keywords     = {{signal-regulated kinase (ERKI/2); extracellular; cerebral blood flow (CBF); cerebral ischemia; subarachnoid hemorrhage (SAH)}},
  language     = {{eng}},
  pages        = {{65--67}},
  publisher    = {{Springer}},
  title        = {{Subarachnoid hemorrhage induces upregulation of vascular receptors and reduction in rCBF via an ERKI/2 mechanism}},
  url          = {{http://dx.doi.org/10.1007/978-3-211-75718-5_12}},
  doi          = {{10.1007/978-3-211-75718-5_12}},
  volume       = {{104}},
  year         = {{2008}},
}