發明
中華民國
101140621
I 561524
茶鹼類衍生物用於腦損傷誘導之神經性疾患USE FOR BRAIN INJURY-INDUCED NEUROPATHIC DISEASES OF XANTHINE DERIVATIVES
高雄醫學大學
2016/12/11
血管鉀離子通道活性之變化,經常與蜘蛛膜下腔出血 (subarachnoid hemorrhage, SAH) 後腦血管功能之異常有關。於分離之基底動脈、血管舒張劑KMUP- 1治療組和KATP 通道活化劑pinacidil之治療組大鼠均呈現正常態之血管反應性。由 KMUP- 1治療組和pinacidil之治療組大鼠,改善蜘蛛膜下腔出血誘發之血管痙攣運動功能和鉀通道之抑制作用。此外,蜘蛛膜似乎修改鉀通道鈣敏感性。KMUP-1 和pinacidil可預防蜘蛛膜下腔出血誘發之痙攣,至少部分是透過恢復大電導性鈣激活鉀離子通道之活性。 Alterations in the activity of vascular K+ channels are commonly associated with abnormalities in cerebral vascular function after subarachnoid hemorrhage. In isolated basilar arteries, KMUP-1-treated and pinacidil-treated rats showed normalized the vascular reactivity. Subarachnoid hemorrhage -induced deficits in motor function and large-conductance Ca2+-activated K+-channel inhibition were improved by KMUP-1-treated and pinacidil-treated rats. Additionally, subarachnoid hemorrhage appears to modify large-conductance Ca2+-activated K+ -channel calcium sensitivity. KMUP-1 and pinacidil prevent subarachnoid hemorrhage-induced vasospasm at least in part by the restoration of BKCa-channel activities.
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