作者: Shaji Philip , William M. Armstead
DOI: 10.1016/S0006-8993(03)02879-8
关键词: Vasodilation 、 Glutamate receptor 、 Superoxide 、 MAPK/ERK pathway 、 Vasoconstriction 、 p38 mitogen-activated protein kinases 、 Protein kinase A 、 Internal medicine 、 NMDA receptor 、 Biology 、 Endocrinology
摘要: Abstract Previous studies in piglets have shown that the generation of oxygen free radicals (O−2) following traumatic brain injury and hypoxia/ischemia contribute to reversal N-methyl- d -aspartate (NMDA)-induced pial artery dilation vasoconstriction. This study determined contribution protein tyrosine kinase (PTK) mitogen-activated (MAPK) activation impairment NMDA cerebrovasodilation by O−2 equipped with a closed window. Exposure cerebral cortex xanthine oxidase generating system (OX) reversed (10−8, 10−6 M) vasoconstriction but such was partially prevented PTK inhibitor, genistein, MAPK (ERK isoform) U0126, (p38 SB203580 (9±1 15±1 vs. −1±1 5±1 9±1% for sham control, OX presence respectively). However, p38 SB203580, dilator significantly less than ERK U0126. Similar results were obtained glutamate. These data show contributes dilation. Furthermore, these indicate differential role brain.