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

将大鼠或小鼠脑内小动脉（ID:5 ~ 10 μm）定位于神经元组织内，用实时计算机视频显微镜连续监测其内径。将脑微血管腔内直径的变化记录在计算机图像文件上，然后用图像软件进行分析。在前列腺素F_<2_α>的收缩过程中，高碳酸血症（PCO_2=50 mmHg）诱导血管舒张，这种舒张被atp敏感的K^+通道拮抗剂格列本脲所消除。左旋克马卡林和KCl可引起脑实质小动脉的血管扩张，而格列本脲或向内整流K^+通道拮抗剂BaCl_2可分别消除这一作用。利多卡因抑制左旋克马卡林的舒张作用，而不抑制KCl的舒张作用。因此，在脑实质小动脉中，atp敏感的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，利多卡因似乎降低了血管舒张介质，主要由atp敏感的K^+通道起作用，而不是由内向整流的K^+通道起作用。KCl可诱导正常（5 ~ 10 mM）和高血压（5 ~ 15 mM）大鼠脑小动脉的血管扩张，而BaCl_2可完全消除这两种大鼠的血管扩张。在高血压大鼠的小动脉中，与正常大鼠的小动脉相比，KCl的血管舒张反应增强。因此，在脑实质小动脉中，慢性高血压患者通过向内整流K^+通道的血管舒张反应似乎增强。异氟醚同时扩张了正常小鼠和神经性一氧化氮合酶敲除小鼠脑切片的脑实质内小动脉，这表明神经性一氧化氮合酶的活性可能不会介导这种麻醉剂的脑血管舒张作用。上述结果表明，K^+通道参与脑实质小动脉血管功能，神经元一氧化氮合酶可能在某些麻醉剂引起的血管扩张作用中不起作用。少

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