Autonomic nervous control of nasal vasculature and airflow resistance in the anaesthetized dog.
Autonomic nervous control of nasal vasculature and airflow resistance in the anaesthetized dog.
复制标题
麻醉狗鼻脉管系统和气流阻力的自主神经控制。
DOI：
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发表时间：
1989
期刊：
影响因子：
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通讯作者：
J. C. Wang
中科院分区：
文献类型：
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作者：
M. A. Lung;J. C. Wang
1. 在戊巴比妥麻醉的双侧鼻黏膜血管灌注恒定的狗中，测量了鼻气道阻力、血管阻力、血管电容（通过静脉总流出量的变化）和前后静脉系统的血流量。2. 电刺激颈交感干、尾鼻神经或腭主神经的外周末端可增加血管阻力，降低血管容量和气道阻力。心得安和阿托品对反应没有影响，而布雷利姆完全消除了它们；酚妥拉明明显降低血管阻力反应，部分降低血管电容和气道反应。因此，交感刺激通过α -肾上腺素能机制引起抵抗血管的收缩，通过α -肾上腺素能机制以及一些非肾上腺素能和非胆碱能机制引起电容血管的收缩。3. 颈交感干、尾鼻神经和腭主神经去神经使鼻血管阻力降低，血管容量和气道阻力增加，提示通过尾鼻神经和腭主神经向鼻黏膜进行张力性交感放电。4. 电刺激翼状管神经降低了血管阻力，但增加了血管电容（后静脉系统）和气道对低压刺激（低于10 V）的阻力，降低了血管电容（前静脉系统）和气道对高压刺激（高于10 V）的阻力。六甲溴铵逆转了高压刺激下的血管阻力反应、血管电容和气道反应。苯妥拉明和苯妥拉明增强了高压刺激下的血管阻力反应，逆转了血管电容和气道阻力反应。因此，低电压刺激导致阻力血管和电容血管的副交感神经扩张，而高电压刺激导致阻力血管的副交感神经扩张和电容血管的交感神经收缩。副交感神经血管扩张是阿托品抵抗，交感神经血管收缩部分是通过α -肾上腺素能机制。5. 翼状管神经的去神经支配不影响血管阻力、血管电容或气道阻力，提示副交感神经和交感神经通过该神经向鼻血管的张力性放电可以忽略不计。6. 同时最佳刺激交感神经和副交感神经导致血管收缩，特别是在电容血管，表明交感神经优于副交感神经的控制。
1. In pentobarbitone‐anaesthetized dogs with constant‐flow vascular perfusion of nasal mucosa on both sides, nasal airway resistance, vascular resistance, vascular capacitance (via changes in total venous outflow) and blood flow in the anterior and posterior venous systems were measured. 2. Electrical stimulation of the cut peripheral ends of the cervical sympathetic trunk, caudal nasal nerve, or major palatine nerve increased vascular resistance and decreased vascular capacitance and airway resistance. Propranolol and atropine had no effect on the responses while bretylium completely abolished them; phentolamine greatly lessened the vascular resistance response and partially decreased the vascular capacitance and airway responses. Hence, sympathetic stimulation causes constriction of the resistance vessels via alpha‐adrenergic mechanism and constriction of capacitance vessels via alpha‐adrenergic as well as some non‐adrenergic and non‐cholinergic mechanisms. 3. Denervation of the cervical sympathetic trunk, caudal nasal nerve and major palatine nerve decreased nasal vascular resistance and increased vascular capacitance and airway resistance, suggesting tonic sympathetic discharge to nasal mucosa via caudal nasal and major palatine nerves. 4. Electrical stimulation of the nerve of pterygoid canal decreased vascular resistance but increased vascular capacitance (in the posterior venous system) and airway resistance to low‐voltage stimulation (below 10 V), and decreased vascular capacitance (in the anterior venous system) and airway resistance to high‐voltage stimulation (above 10 V). Hexamethonium reversed the vascular resistance response as well as vascular capacitance and airway responses to high‐voltage stimulation. Bretylium and phentolamine enhanced the vascular resistance response and reversed vascular capacitance and airway resistance responses to high‐voltage stimulation. Hence, low‐voltage stimulation results in parasympathetic dilatation of resistance and capacitance vessels whereas high‐voltage stimulation results in parasympathetic dilatation of resistance vessels and sympathetic constriction of capacitance vessels. The parasympathetic vasodilatation was atropine resistance and the sympathetic vasoconstriction was partially via alpha‐adrenergic mechanisms. 5. Denervation of the nerve of pterygoid canal did not affect vascular resistance, vascular capacitance or airway resistance suggesting negligible tonic parasympathetic and sympathetic discharges to nasal blood vessels via the nerve. 6. Simultaneous optimal stimulation of sympathetic and parasympathetic nerves resulted in vasoconstriction, especially in capacitance vessels, suggesting sympathetic predominance over parasympathetic control.