Advanced

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 In Cerebral Vasospasm: New Strategies in Research and Treatment 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)
Please use this url to cite or link to this publication:
author
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)
in
Cerebral Vasospasm: New Strategies in Research and Treatment
volume
104
pages
65 - 67
publisher
Springer
conference name
9th International Conference on Cerebral Vasospasm
external identifiers
  • wos:000256013000012
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
2009-06-03 10:44:24
date last changed
2016-04-15 23:36:40
@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},
  keyword      = {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},
  volume       = {104},
  year         = {2008},
}