Abstract：
:N-Methyl-D-aspartate (NMDA)-induced pial artery dilation is reversed to vasoconstriction following fluid percussion brain injury (FPI). This study investigated the contribution of activation of protein tyrosine kinase (PTK) and the extracellular signal-regulated kinase (ERK) and p38 isoforms of mitogen-activated protein kinase (MAPK) in impaired vasodilation to NMDA after fluid percussion brain injury in pigs equipped with a closed cranial window. NMDA (10(-8), 10(-6) M)-induced vasodilation was reversed to vasoconstriction following fluid percussion brain injury, but such responses were partially restored by genistein (4',5,7-trihydroxy isoflavone), U0126 [1,4-diamino-2,3-dicyano-1,4-bis (0-aminophenylmercapto)butadiene] and SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole], PTK, ERK and p38 MAPK inhibitors (9+/-1% and 16+/-1%, sham control; -6+/-2% and -11+/-3%, fluid percussion brain injury; and 3+/-1% and 6+/-1%, fluid percussion brain injury-genistein, respectively). However, the robustness of the protection to NMDA dilation was significantly greater for U0126 vs. SB203580 (4+/-1% and 7+/-1% vs. 1+/-1% and 1+/-2%). Similar results were observed for glutamate. These data show that PTK, ERK and p38 MAPK activation contribute to impaired NMDA cerebrovasodilation after fluid percussion brain injury. These data suggest that activation of the ERK isoform of MAPK contributes to such impairment more than the p38 MAPK isoform.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Armstead WMdoi
10.1016/s0014-2999(03)02012-0keywords:
subject
Has Abstractpub_date
2003-08-08 00:00:00pages
249-54issue
2-3eissn
0014-2999issn
1879-0712pii
S0014299903020120journal_volume
474pub_type
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