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臂旁核区域的激活引发神经源性介导的冠状动脉收缩。

Activation in the region of parabrachial nucleus elicits neurogenically mediated coronary vasoconstriction.

作者信息

Miller F J, Marcus M L, Brody M J, Gutterman D D

机构信息

Department of Internal Medicine, University of Iowa, Iowa City 52242.

出版信息

Am J Physiol. 1991 Nov;261(5 Pt 2):H1585-96. doi: 10.1152/ajpheart.1991.261.5.H1585.

DOI:10.1152/ajpheart.1991.261.5.H1585
PMID:1683174
Abstract

A role for parabrachial nucleus in cardiovascular regulation is suggested by evidence that electrical stimulation in this region elicits increase in heart rate and arterial pressure. We hypothesized that parabrachial nucleus may also be involved in control of coronary vasomotor tone. After beta-adrenergic receptor blockade in anesthetized cats, electrical stimulation in the region of parabrachial nucleus produced no change in heart rate, an increase in arterial pressure (34 +/- 6 mmHg), and a transient reduction in coronary blood flow velocity (-21 +/- 2%). Coronary resistance (72 +/- 9%) and femoral resistance (189 +/- 31%) increased markedly. The decrease in coronary blood flow velocity was abolished by stellate ganglionectomy or alpha 1-adrenergic blockade without altering pressor or femoral responses. Injection of the neurotransmitter L-glutamate or kainic acid into parabrachial nucleus also elicited coronary vasoconstriction. We conclude that electrical or chemical activation in the region of parabrachial nucleus elicits coronary vasoconstriction as part of a generalized sympathetic activation. The fact that the coronary response is elicited by chemical activation suggests that cell bodies in the region of medial parabrachial nucleus and subceruleus, as opposed to fibers of passage, are involved in this central neural coronary vasoconstriction.

摘要

臂旁核在心血管调节中的作用可由以下证据表明

该区域的电刺激会引起心率和动脉压升高。我们推测臂旁核可能也参与冠状动脉血管舒缩张力的控制。在麻醉猫中进行β-肾上腺素能受体阻断后,臂旁核区域的电刺激未引起心率变化,但动脉压升高(34±6 mmHg),冠状动脉血流速度短暂降低(-21±2%)。冠状动脉阻力(72±9%)和股动脉阻力(189±31%)显著增加。星状神经节切除术或α1-肾上腺素能阻断可消除冠状动脉血流速度的降低,而不改变升压反应或股动脉反应。向臂旁核注射神经递质L-谷氨酸或 kainic 酸也会引起冠状动脉血管收缩。我们得出结论,臂旁核区域的电或化学激活会引起冠状动脉血管收缩,这是全身性交感神经激活的一部分。化学激活引发冠状动脉反应这一事实表明,与传导纤维相反,臂旁核内侧区域和蓝斑下核的细胞体参与了这种中枢神经性冠状动脉血管收缩。

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Activation in the region of parabrachial nucleus elicits neurogenically mediated coronary vasoconstriction.臂旁核区域的激活引发神经源性介导的冠状动脉收缩。
Am J Physiol. 1991 Nov;261(5 Pt 2):H1585-96. doi: 10.1152/ajpheart.1991.261.5.H1585.
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引用本文的文献

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A role for the lateral parabrachial nucleus in cardiovascular function and fluid homeostasis.外侧臂旁核在心血管功能和体液平衡中的作用。
Front Physiol. 2014 Nov 18;5:436. doi: 10.3389/fphys.2014.00436. eCollection 2014.
2
A review of neuroimaging studies of stressor-evoked blood pressure reactivity: emerging evidence for a brain-body pathway to coronary heart disease risk.应激源诱发的血压反应性的神经影像学研究综述:冠心病风险脑-身通路的新证据
Neuroimage. 2009 Sep;47(3):922-36. doi: 10.1016/j.neuroimage.2009.04.073. Epub 2009 May 4.
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Individual differences in stressor-evoked blood pressure reactivity vary with activation, volume, and functional connectivity of the amygdala.
应激源诱发的血压反应性的个体差异随杏仁核的激活、体积和功能连接性而变化。
J Neurosci. 2008 Jan 23;28(4):990-9. doi: 10.1523/JNEUROSCI.3606-07.2008.