Is a trigeminal nociception-induced cardiovascular response related to the trigemino-vagal reflex?

三叉神经伤害感受诱发的心血管反应与三叉神经迷走神经反射有关吗?

基本信息

  • 批准号:
    10671883
  • 负责人:
  • 金额:
    $ 2.43万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    1998
  • 资助国家:
    日本
  • 起止时间:
    1998 至 2001
  • 项目状态:
    已结题

项目摘要

We studied effects of electrical stimulation of the inferior alveolar nerve (IAN) and medulla on arterial blood pressure (ABP) in cats. Electrical stimulation of dorsomedial medulla, infratrigeminal nucleus (IFT) and the rostral ventrolateral medulla (RVLM) which has neurons labeled retrogradely by injection of WGA HRP into the unilateral substantia intermedia lateralis of the thoracical spinal cord and containing phenylethanolamine-N-methyl transferaseinduced significant vasopressor response. Vasopressor response on IFT always mimics vasopressor response on IAN. Vasodepressor responses induced when the caudal ventrolateral medulla just ventral to ambiguus nucleus, lateral tegmental field, the trigeminal nucleus interpolaris, trigeminal spinai tract and paramedian reticular nucleus were stimulated. However these vasodepressor responses did not similar to vasodepressor response on TDR and could be almost vagal induced cardio-vascular response. Only after spinalization and electrical stimulation of RVLM lesion, basal ABP decreased and TDR completely disappeared. In medulla, the distribution of possible inhibitory synaptic ligands was mapped using immunohistochemical techniques. It demonstrated that noradrenergic, glycinergic and GABAergic neurons and neurons for adrenaliine α2A receptor, GABAA, GABAB and glycine receptors were also distributed along the sympatho-reflexive route including RVLM and IFT etc. These results suggest that TDR may be negative feedback response to sympathetic nervous system, readily induced by noxious stimulation in the trigeminal region whenever basal ABP and HR are high and that TDR is induced by inhibiting vasoexciting centrer, RVLM through trigeminal nucleus and reticular formation.
研究电刺激猫下牙槽神经(Ian)和延髓对动脉血压(ABP)的影响。电刺激延髓背内侧、三叉神经下核(IFT)和延髓头端腹外侧区(RVLM),将WGA-HRP逆行标记的神经元注入一侧胸髓中间质,并含有苯乙醇胺-N-甲基转移酶,可引起明显的血管加压反应。IFT的升压反应总是与Ian的升压反应相似。刺激延髓尾侧腹外侧区至疑核腹侧、被盖外侧区、三叉神经内侧核、三叉神经脊束核和三叉神经旁网状核均可引起血管降压反应。然而,这些血管降压反应与TDR上的血管降压反应不同,可能几乎是迷走神经引起的心血管反应。仅在脊髓化和电刺激RVLM损伤后,基础ABP下降,TDR完全消失。在延髓,可能的抑制性突触配体的分布被用免疫组织化学技术绘制。结果表明,去甲肾上腺素能神经元、甘氨酸能神经元和GABA能神经元以及肾上腺素α-A受体、GABA受体、GABA受体和甘氨酸受体神经元也沿交感反射通路分布,提示TDR可能是交感神经系统的负反馈反应,当基础血压和心率较高时,三叉神经区伤害性刺激容易诱发TDR,TDR是通过三叉神经核和网状结构抑制血管兴奋中枢RVLm而产生的。

项目成果

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NAKAJO Nobuyoshi其他文献

NAKAJO Nobuyoshi的其他文献

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{{ truncateString('NAKAJO Nobuyoshi', 18)}}的其他基金

The effects of anesthetics on aquaporin-5
麻醉药对水通道蛋白5的影响
  • 批准号:
    17592087
  • 财政年份:
    2005
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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