2000 Fiscal Year Final Research Report Summary
A STUDY FOR INTRACELLULAR CALCIUM REGULATING MECHANISMS IN ARTERIAL SMOOTH MUSCLE AND THE EFFECT OF ANESTHETICS ON THESE MECHANISMS
| 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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| Keywords | CEREBRAL ARTERIAL SMOOTH MUSCLE / Ca2_+ / K_+ / VOLATILE ANESTHETICS / LOCAL ANESTHETICS |
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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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