The research regarding the function of cerebral microvasculature using gene-knockout animals and the role of anesthetic drugs
The research regarding the function of cerebral microvasculature using gene-knockout animals and the role of anesthetic drugs
批准号:
13470327
负责人:
HATANO Yoshio
金额:
$9.34万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2001
资助国家:
日本
项目状态:
已结题
起止时间:
2001 至 2004
中文摘要
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英文摘要
Intraparenchymal arterioles (ID:5-10 μm) in the rat or mouse brain slices were located within the neuronal tissue, and their internal diameters were continuously monitored with the live computerized videomicroscopy. Changes of intraluminal diameter in cerebral microvessels were recorded on computer image files and then analyzed using the image software.During contraction to prostaglandin F_<2_α>, hypercapnia (PCO_2=50 mmHg) induced vasodilation, which is abolished by an ATP-sensitive K^+ channel antagonist glibenclamide. Levcromakalim and KCl produced the vasodilation of the cerebral parenchymal arterioles, which is abolished by glibenclamide or an inward rectifier K^+ channel antagonist BaCl_2, respectively. Lidocaine inhibited the dilation produced by levcromakalim, but not by KCl. Therefore, in cerebral parenchymal arterioles, ATP-sensitive K^+ channels play a major role in vasodilator responses produced by mild hypercapnia. In addition, lidocaine appears to reduce vasodilation medi … More ated by ATP-sensitive K^+ channels, but not by inward rectifier K^+ channels.Addition of KCl induced vasodilation of normotensive (5 to 10 mM) and hypertensive (5 to 15 mM) rat cerebral arterioles, whereas BaCl_2 completely abolished the vasodilation in both strains. In arterioles of hypertensive rats, vasodilator responses to KCl were augmented compared with those in normotensive rat arterioles. Thus, in cerebral parenchymal arterioles, the vasodilator response via inward rectifier K^+ channels appears to be augmented in chronic hypertension.Isoflurane simultaneously dilated intraparenchymal arterioles in brain slices from normal as well as neuronal nitric oxide synthase knockout mice, indicating that activity of neuronal nitric oxide synthase may not mediate the cerebral vasodilator effect of this anesthetic.Above results indicate that K^+ channels contribute to vascular function of cerebral parenchymal arterioles and that neuronal nitric oxide synthase may not play a role in vasodilator effect induced by some anesthetics. Less
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Ogawa K, Yamada S.Mizumoto K, I Iranami H, Hatano Y: "Inhibitory effects of halothane, isoflurarie, sevoflurane, and pentobarbital on the constriction induced by I hypocapnia and bicarbonate in isolated canine cerebral arteries"Jounal Neurosurg Anesthesio
小川 K、山田 S.水本 K、伊拉纳米 H、波多野 Y:“氟烷、异氟烷、七氟烷和戊巴比妥对犬离体脑动脉中由低碳酸血症和碳酸氢盐引起的收缩的抑制作用”《神经外科麻醉杂志》
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作者:
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通讯作者:
Kinoshita H, Iranami H, Kimoto Y, Dojo M, Hatano Y: "Mild alkilinization and acidification differentially modify the effects of lidocaine or mexiletine on vasorelaxation mediated by ATP-sensitive K^+ channels"Anesthesiology. 95. 200-206 (2001)
Kinoshita H、Iranami H、Kimoto Y、Dojo M、Hatano Y:“轻度碱化和酸化不同地改变了利多卡因或美西律对 ATP 敏感 K^ 通道介导的血管舒张的影响”麻醉学。
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Ogawa K.Yamamoto M, Mizumoto K, Hatano Y: "Volatile anesthestics attenuate hypocapnia-induced constriction in isolated dog cerebral arteries"Canadian Jounal of Anesthesia. 44(4). 426-432 (1997)
Okawa K.Yamamoto M、Mizumoto K、Hatano Y:“挥发性麻醉剂可减轻离体狗脑动脉中低碳酸血症引起的收缩”《加拿大麻醉杂志》。
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Lidocaine impairs vasodilation mediated by adenosine triphosphate-sensitive K^+ channels but not by inward rectifier K^+ channels in parenchymal microvessels of rat cerebral cortex.
利多卡因损害大鼠大脑皮层实质微血管中由三磷酸腺苷敏感K 通道介导的血管舒张,但不损害内向整流K 通道介导的血管舒张。
DOI:
--
发表时间:
2004
期刊:
Anesth Analg 99
影响因子:
--
作者:
[Kinoshita H, Nakahata K, Dojo M, Kimoto Y, Hatano Y]
通讯作者:
Hatano Y
The inhibitory effects of isoflurane on protein tyrosine phosphorylation-modulated contraction of rat aortic smooth muscle
异氟烷对蛋白酪氨酸磷酸化调节的大鼠主动脉平滑肌收缩的抑制作用
DOI:
--
发表时间:
2004
期刊:
Anesthesiology 101:6
影响因子:
--
作者:
[Yu J, Ogawa K, Tokinaga Y, Mizumoto K, Kakutani T, Hatano Y]
通讯作者:
Hatano Y
共 36 条
The analysis of coronary arterial vasospasm using the live-cell imaging in genetically modified pigs and effects of anesthetics
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批准号:17390432
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$10.24万
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财政年份:2005
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负责人:HATANO Yoshio
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依托单位:
A STUDY FOR INTRACELLULAR CALCIUM REGULATING MECHANISMS IN ARTERIAL SMOOTH MUSCLE AND THE EFFECT OF ANESTHETICS ON THESE MECHANISMS
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批准号:10470324
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项目类别:Grant-in-Aid for Scientific Research (B).
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资助金额:$4.8万
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财政年份:1998
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负责人:HATANO Yoshio
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依托单位:
Effect of volatile anesthetics on the ion-channels of the cerebral vascular smooth muscle isolated from dog
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批准号:07457361
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$4.74万
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财政年份:1995
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负责人:HATANO Yoshio
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依托单位:
EFFECTS OF ANESTHETICS ON HYPOCAPNIA-INDUCED CONTRACTION OF ISOLATED CEREBRAL ARTERY
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批准号:03454374
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$4.16万
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财政年份:1991
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负责人:HATANO Yoshio
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依托单位:
Organ Specificity in the responses of isolated arteries to anesthetics.
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批准号:63570722
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.41万
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财政年份:1988
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负责人:HATANO Yoshio
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依托单位:
海外基金