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The role of the vestibulosympathetic reflex in blood pressure regulation in humans.

机译：前庭交感神经反射在人类血压调节中的作用。

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Abstract Chapter 2. Activation of the vestibular otolith organs with head-down rotation increases muscle sympathetic nerve activity (MSNA) in humans. Previously, we demonstrated this vestibulosympathetic reflex (VSR) elicits increases in MSNA during baroreflex unloading (i.e., lower-body negative pressure) in humans. Whether such an effect persists during baroreflex loading is unknown. We tested the hypothesis that the ability of the VSR to increase MSNA is preserved during baroreflex unloading and inhibited during baroreflex loading. Ten subjects (26+/-1 yr) performed 3 trials of head-down rotation (HDR) to activate the VSR. These trials were performed after a period of sustained saline (control), nitroprusside (baroreflex unloading: 0.8-1.0 mug/kg/min), and phenylephrine (baroreflex loading: 0.6-0.8 mug/kg/min) infusion. Nitroprusside infusion decreased (Delta7+/-1 mmHg; p0.001) and phenylephrine infusion increased (Delta8+/-1 mmHg; p0.001) mean arterial pressure at rest. HDR performed during the control (Delta3+/-2 bursts/min, Delta314+/-154 arbitrary units (au) total activity, Delta41+/-18% total activity; p0.05) and nitroprusside trials (Delta5+/-2 bursts/min, Delta713+/-241 au total activity, Delta49+/-20% total activity; p0.05) increased MSNA similarly despite significantly elevated levels at rest (13+/-2 to 26+/-3 bursts/min) in the latter. In contrast, HDR performed during the phenylephrine trial failed to increase MSNA (Delta0+/-1 bursts/min, Delta-15+/-33 au total activity, Delta-8+/-21% total activity). These results confirm previous findings that the ability of the VSR to increase MSNA is preserved during baroreflex unloading. In contrast, the ability of the VSR to increase MSNA is abolished during baroreflex loading. These results provide further support for the concept that the VSR may act primarily to defend against hypotension in humans.;Abstract Chapter 3. Orthostatic intolerance is a common problem following bed rest. The mechanism for this is equivocal. Vestibular reflexes contribute to orthostatic blood pressure regulation. We hypothesized that sympathetic nerve responses to otolith stimulation would be attenuated by prolonged head-down bed rest (HDBR) and that this attenuation would be associated with increased orthostatic intolerance. Arterial blood pressure, heart rate, muscle sympathetic nerve activity (MSNA), and peripheral vascular conductance were measured during head-down rotation (HDR; otolith organ stimulation) in the prone posture before and after short-duration (24-hrs; n=22) and prolonged (36+/-1 days; n=8) HDBR. Head-up tilt at 80° was performed to assess orthostatic tolerance. After short-duration HDBR, MSNA responses to HDR were preserved (Delta5+/-1 bursts/min, Delta53+/-13% burst frequency, Delta65+/-13% total activity; p0.001). No association was observed between the vestibulosympathetic reflex and head-up tilt duration. After prolonged HDBR, MSNA responses to HDR were attenuated ∼50%. MSNA increased by Delta23+/-13% burst frequency and Delta34+/-22% total activity during HDR. Moreover, these results were observed in 3 subjects tested again at 75+/-1 days of HDBR. This reduction in MSNA responses to otolith organ stimulation at 5 weeks was associated with reductions in head-up tilt duration. These results indicate that prolonged HDBR (∼5 wks) attenuates the vestibulosympathetic reflex and contributes to orthostatic intolerance following HDBR in humans. These results suggest a novel mechanism in the development of orthostatic intolerance in humans.;Abstract Chapter 4. Classically, the glycerol dehydration test (GDT) has been used to test for the presence of Meniere's disease and can cause acute alterations in vestibular reflexes in both normal and pathological states. The vestibulosympathetic reflex (VSR) elicits increases in muscle sympathetic nerve activity (MSNA) and peripheral vasoconstriction. We hypothesized that the GDT would attenuate the VSR through an acute fluid shift of the inner ear. Nine male subjects (27+/-1 years) performed head-down rotation (HDR), which engages the VSR, before and after administration of either the GDT or saline. MSNA (microneurography), arterial blood pressure, and leg blood flow (venous occlusion plethysmography) were measured during HDR. Before drug administration, HDR significantly increased MSNA in burst frequency (Delta5+/-1 bursts/min, Delta8+/-1 bursts/min; p0.01) and total activity (Delta44+/-13%, Delta77+/-17%; p0.01), and decreased calf vascular conductance (Delta15+/-6%, Delta20+/-3%; p0.01), in both the saline and glycerol trials, respectively. Post-saline, HDR still significantly increased MSNA (Delta6+/-2 bursts/min, Delta83+/-20% total activity; p0.01) and decreased calf vascular conductance (Delta21+/-4%, p0.01), which was not significantly different from pretesting. In contrast, post-GDT resulted in an attenuation of MSNA (Delta3+/-1 bursts/min, Delta22+/-3% total activity) and reduction in calf vascular conductance (Delta7+/-4%) during HDR. These results suggest that a fluid shift of the inner ear via glycerol dehydration attenuates the VSR. These data provide support that dynamic fluid shifts can have a significant effect on the VSR.
机译：摘要第2章。头向下旋转激活前庭耳石器官会增加人类的肌肉交感神经活动（MSNA）。以前，我们证明了这种前庭交感神经反射（VSR）在人体压力反射卸载（即下半身负压）过程中引起MSNA升高。这种作用是否在压力反射负荷期间是否持续尚不清楚。我们测试了以下假设：VSR增加MSNA的能力在压力反射卸载过程中得以保留，而在压力反射加载过程中受到抑制。十名受试者（26 +/- 1岁）进行了3次头向下旋转（HDR）激活VSR的试验。这些试验是在持续输注盐水（对照组），硝普钠（负压负荷：0.8-1.0杯/公斤/分钟）和去氧肾上腺素（压负荷负荷：0.6-0.8杯/公斤/分钟）后进行的。静息时的平均动脉压减少了硝普钠的输注（Delta7 +/- 1 mmHg; p <0.001），而去氧肾上腺素的输注增加了（Delta8 +/- 1 mmHg; p <0.001）。在对照组（Delta3 +/- 2爆发/分钟，Delta314 +/- 154任意单位（au）总活性，Delta41 +/- 18％总活性; p <0.05）和硝普钠试验（Delta5 +/- 2爆发/分钟， Delta713 +/- 241 au总活性，Delta49 +/- 20％总活性； p <0.05）类似地增加了MSNA，尽管后者的静息水平显着升高（13 +/- 2至26 +/- 3猝发/分钟）。相反，在去氧肾上腺素试验期间进行的HDR未能增加MSNA（Delta0 +/- 1突发/分钟，Delta-15 +/- 33 au总活性，Delta-8 +/- 21％总活性）。这些结果证实了以前的发现，即在压力感受器卸载过程中保留了VSR增加MSNA的能力。相反，在压力反射负荷期间，VSR增加MSNA的能力被取消。这些结果为VSR可能主要起到抵御人类低血压的作用的概念提供了进一步的支持。摘要第三章卧床休息后，体位不耐症是一个普遍的问题。这种机制是模棱两可的。前庭反射有助于体位血压的调节。我们假设长时间的低头卧床休息（HDBR）将减弱对耳石刺激的交感神经反应，并且这种衰减将与体位性耐受性增加有关。在短时间（24小时）前后俯卧姿势下，头朝下旋转（HDR；耳石器官刺激）期间测量动脉血压，心率，肌肉交感神经活动（MSNA）和周围血管电导。 22），并延长（36 +/- 1天； n = 8）HDBR。进行80°抬头俯仰以评估体位耐受性。短期HDBR后，保留了MSNA对HDR的响应（Delta5 +/- 1突发/分钟，Delta53 +/- 13％突发频率，Delta65 +/- 13％总活性； p <0.001）。在前庭交感神经反射和抬头持续时间之间未发现关联。延长HDBR后，MSNA对HDR的反应减弱了约50％。在HDR期间，MSNA的爆发频率增加了Delta23 +/- 13％，总活动增加了Delta34 +/- 22％。此外，在HDBR 75 +/- 1天时再次测试的3名受试者中观察到了这些结果。在5周时，对耳石器官刺激的MSNA反应的这种减少与抬头向上倾斜持续时间的减少有关。这些结果表明，延长的HDBR（〜5 wks）会减弱人类的前庭交感神经反射，并导致HDBR后的体位性不耐受。这些结果表明了人类直立性不耐受的发展的新机制。；摘要第4章。经典的甘油脱水试验（GDT）已用于测试美尼尔氏病的存在，并可能导致两种前庭反射的急性改变。正常和病理状态。前庭交感神经反射（VSR）引起肌肉交感神经活性（MSNA）和周围血管收缩的增加。我们假设GDT将通过内耳的急性液体移位来减弱VSR。在服用GDT或生理盐水之前和之后，有9位男性受试者（27 +/- 1岁）进行了头向下旋转（HDR），该旋转参与了VSR。在HDR期间测量MSNA（微神经造影），动脉血压和腿部血流（静脉阻塞体积描记法）。在给药之前，HDR显着增加了MSNA的猝发频率（Delta5 +/- 1猝发/分钟，Delta8 +/- 1猝发/分钟； p <0.01）和总活性（Delta44 +/- 13％，Delta77 +/- 17％； p <分别在盐水和甘油试验中均降低了0.01），并降低了小腿血管的电导率（Delta15 +/- 6％，Delta20 +/- 3％; p <0.01）。盐水后，HDR仍显着增加MSNA（Delta6 +/- 2突增/分钟，Delta83 +/- 20％的总活性； p <0.01）和降低的小腿血管电导率（Delta21 +/- 4％，p <0.01），但没有与预测试有很大的不同。相反，GDT后导致MSNA衰减（Delta3 +/- 1突发/分钟，Delta22 +/- 3％的总活性）和HDR期间小腿血管电导率的降低（Delta7 +/- 4％）。这些结果表明，通过甘油脱水引起的内耳流体移位会减弱VSR。这些数据提供了动力流体动态变化对VSR有重大影响的支持。

著录项

  • 作者

    Dyckman, Damian Joseph.;

  • 作者单位

    The Pennsylvania State University.;

  • 授予单位 The Pennsylvania State University.;
  • 学科 Health Sciences Medicine and Surgery.;Biology Physiology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 190 p.
  • 总页数 190
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

  • 入库时间 2022-08-17 11:38:19

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