| Project/Area Number |
10470324
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | WAKAYAMA MEDICAL COLLEGE |
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Principal Investigator |
HATANO Yoshio WAKAYAMA MEDICAL COLLEGE, DEPARTMENT OF ANESTHESIOLOGY, PROFESSOR AND CHAIRMAN, 医学部, 教授 (70115913)
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| Co-Investigator(Kenkyū-buntansha) |
MAEDA Hiroshi WAKAYAMA MEDICAL COLLEGE, DEPARTMENT OF ANESTHESIOLOGY, INSTRUCTOR, 医学部, 助手 (80199629)
MIZUMOTO Kazuhiro WAKAYAMA MEDICAL COLLEGE, DEPARTMENT OF ANESTHESIOLOGY, INSTRUCTOR, 医学部, 助手 (50239258)
OGAWA Koji WAKAYAMA MEDICAL COLLEGE, DEPARTMENT OF ANESTHESIOLOGY, INSTRUCTOR, 医学部, 助手 (30204077)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥7,500,000 (Direct Cost: ¥7,500,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥5,600,000 (Direct Cost: ¥5,600,000)
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| Keywords | CEREBRAL ARTERIAL SMOOTH MUSCLE / Ca2_+ / K_+ / VOLATILE ANESTHETICS / LOCAL ANESTHETICS / 脳動脈 / 麻酔薬 / Ca^<2+>(カルシウムイオン) / イオンチャネル / 一酸化窒素 / レブクロマカリム / ATP感受性カリウムチャネル / グリベンクラミド / ハロタン / 脳微小血管 / 腸間膜動脈平滑筋 |
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| Research Abstract |
The purpose of this study was to clarify the role of K^+ channels in vasodilator as well as constrictor responses, which regulate intracellular levels of Ca^<2+>, and to determine whether anesthetics may modify these vascular responses via K^+ channels in parenchymal cerebral arterioles.
The studies on cerebral parenchymal arterioles in the rat brain slice were introduced. Halothane dilated cerebral arterioles contracted with prostaglandine F_<2α>. An ATP-sensitive K^+ channel opener, levcromakalim and calcitonin-gene related peptide dilated these arterioles, whereas an ATP-sensitive K^+ channel inhibitor glibenclamide abolished these vasodilator responses. A local anesthetic lidocaine inhibited vasodilation induced by levcromakalim, whereas it did not alter contraction in response to prostaglandine F_<2α>. Lidocaine did not affect vasodilation induced by a nitric oxide donor sodium nitroprusside.
It appears that lidocaine may be selectively capable of inhibiting vasodilaiton mediated by ATP-sensitive K^+ channel s in cerebral parenchymal arterioles. These results suggest that anesthetics may modify the mechanisms to maintain cerebral blood flow by inducing vasodilation mediated by opening of ATP-sensitive K^+ channels, resulting in lowered intracellular levels of Ca^<2+>.
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