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The research regarding the function of cerebral microvasculature using gene-knockout animals and the role of anesthetic drugs

基因敲除动物脑微血管功能及麻醉药物作用的研究

基本信息

批准号：
13470327
负责人：
HATANO Yoshio
金额：
$ 9.34万
依托单位：
Wakayama Medical University
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
起止时间：
2001 至 2004
项目状态：
已结题

项目摘要

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

大鼠或小鼠脑切片中的实质内小动脉（ID：5-10 μm）位于神经元组织内，并使用实时计算机视频显微镜连续监测其内径。在前列腺素F_（2_α）收缩过程中，高碳酸血症（PCO_2=50 mmHg）引起血管舒张，ATP敏感性K^+通道拮抗剂格列本脲可阻断这种舒张作用。左克罗卡林和KCl使脑实质小动脉血管舒张，格列本脲或内向整流性K^+通道拮抗剂BaCl_2可分别阻断这一作用。利多卡因抑制左克罗卡林产生的扩张，但不抑制KCl。因此，在脑实质小动脉中，ATP敏感性K^+通道在轻度高碳酸血症引起的血管舒张反应中起主要作用。此外，利多卡因似乎减少血管舒张介质， ...更多信息加入KCl可引起正常血压（5 - 10 mM）和高血压（5 - 15 mM）大鼠脑小动脉的舒张，而BaCl_2则完全消除了这两种品系大鼠脑小动脉的舒张。在高血压大鼠的小动脉中，血管舒张反应KCl增强与正常大鼠的小动脉相比。因此，在脑实质小动脉中，通过内向整流性K^+通道的血管舒张反应似乎在慢性高血压中增强。异氟烷同时扩张正常小鼠和神经元型一氧化氮合酶敲除小鼠脑切片中的脑实质内小动脉，提示神经元型一氧化氮合酶活性可能不介导该麻醉药的脑血管舒张作用，上述结果提示K^+神经元型一氧化氮合酶可能在某些麻醉药引起的血管扩张效应中不起作用。少