延髓上部位对动脉压力和局部血流动力学的强直控制。

B F Cox, M J Brody
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引用次数: 3

摘要

我们检查了在正常和减少潮汐量下,脑桥部位在血管舒缩张力的强直控制中的作用。在Kölliker-Fuse核(KFN)水平向脑桥微注射利多卡因。注射分别在双侧硬脑膜下6、7、8和9 mm以及中线外侧0.9和2.5 mm处进行。利多卡因使KFN在正常和减少潮气量时平均动脉压(MAP)下降(-14 mmHg)。这些影响主要是由后躯血管阻力的降低介导的。利多卡因进入腹内侧部位(硬脑膜下8.0 mm,中线外侧0.9 mm)通过增加肾、肠系膜和后躯血管阻力而增加MAP。经椎动脉脱突(SAD)后,潮汐容量的减少增加了加压作用,减弱了将利多卡因注射到脑桥腹内侧(硬脑膜下9.0 mm,中线外侧0.9 mm)时的心动过速反应。SAD还增强了脑桥腹内侧注射利多卡因后的升压反应。这项工作证明了髓上部位在血管舒缩性张力的强直控制中的作用。
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Tonic control of arterial pressure and regional hemodynamics by supra-medullary sites.

We examined the role of pontine sites in the tonic control of vasomotor tone under normal and reduced tidal volumes. Lidocaine was microinjected in pons at the level of the Kölliker-Fuse nucleus (KFN). Injections were made bilaterally 6, 7, 8, and 9 mm below dura, and 0.9 and 2.5 mm lateral to midline. Lidocaine in KFN produced a fall (-14 mmHg) in mean arterial pressure (MAP) at normal and reduced tidal volumes. These effects were mediated primarily by a reduction in hindquarter vascular resistance. Lidocaine into a ventromedial site (8.0 mm beneath dura, 0.9 mm lateral to midline) increased MAP by increasing renal, mesenteric, and hindquarter vascular resistance. After sino-aortic deafferentation (SAD), reduced tidal volume augmented the pressor and blunted the tachycardic responses to lidocaine injected into the ventromedial pons (9.0 mm beneath dura, 0.9 mm lateral to midline). SAD also enhanced the pressor response to lidocaine injected into ventromedial pons. This work demonstrates a role for supra-medullary sites in the tonic control of vasomotor tone.

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