副交感神经刺激对猫鼻粘膜血流调节物神经肽释放的影响

为了解鼻粘膜副交感神经刺激对末梢神经肽释放粘膜血流变化的影响，用激光多普苗血流计观察副交感神经刺激对猫鼻粘膜血流变化的调控作用，并用放射免疫学方法检测静脉血血管活性肠肽（ＶＩＰ）水平变化。结果表明：电刺激鼻粘膜副交感神经可以引起鼻粘膜阿托品抵抗型血管扩张，血流信号增加，同时伴静脉血ＶＩＰ水平增高，且随刺激的时间而变化，这种血管扩张作用与阿托品敏感型腺体分泌作用机制不同，提示刺激引起的鼻粘膜副交感神     

电刺激蝶腭神经节对鼻粘膜血流的调控作用

为了解蝶腭神经节在鼻粘膜血流调节中的作用，应用激光多普勒血流仪观察刺激蝶腭神经节对猫鼻粘膜血流变化的调控作用。结果表明，电刺激一侧蝶腭神经节可以引起双侧鼻粘膜血管扩张，血流增加，并产生喷嚏反射，这种反应依电刺激的强度、频率而异，且与刺激时间有关。电刺激一侧副交感神经（切除颈上交感神经节的翼管神经）远侧游离端，只引起同侧血管反应。提示刺激蝶腭神经节引起的血管反应可能是通过中枢反射机制起作用。实验还显示刺激蝶腭神经节具有“反向血流调节作用”，这种调节作用的机制有待于进一步研究。     

电刺激蝶腭神经节对鼻粘膜血流的调控作用

为了解蝶腭神经节在鼻粘膜血流调节中的作用，应用激光多普勒血流仪观察刺激蝶腭神经节对猫鼻粘膜血流变化的调控作用，结果表明，电刺激一侧蝶腭神经节可以引起双侧鼻粘膜血管扩张，血流增加，并产生喷嚏反应，这种反应依电刺激的强度，频率而异，且与刺激时间有关。     

蝶腭神经节电刺激对猫鼻粘膜神经末梢VIP释放的影响

为了解蝶腭神经节刺激对鼻粘膜神经肽释放的调节机制，用免疫组织细胞化学技术（ＡＢＣ法）及放射免疫学方法观察电刺激蝶腭神经节对猫鼻粘膜神经末梢血管活性肠肽（ＶＩＰ）释放的影响。实验显示，蝶腭神经节刺激后，鼻粘膜静脉血浆ＶＩＰ在１５秒钟达高峰，随时间变化而逐渐下降。于此同时，分布于小动脉壁、小静脉壁、腺泡周围上皮细胞间的ＶＩＰ免疫反应阳性物质明显较神经节刺激前增多。实验结果表明蝶腭神经节刺激可促进猫鼻粘     

血管活性肠肽(VIP)、P物质(SP)及胃肠多肽(BFP)在鼻息肉中的表达

文献中虽已对不同物种（包括人类）正常鼻粘膜神经介质、神经激素的解剖学分布有所描述，但尚缺少有关鼻息肉兔疫组织化学的研究。该文所研究的三种神经肽中，ＳＰ和ＢＦＰ都由感觉神经所释放，它们可引起血管扩张、血浆外渗和腺体分泌，且ＢＦＰ还可能是生长因子；而ＶＩＰ定位于副交感神经元，它亦可促使血管扩张和腺体分泌，并有增强ＳＰ的血浆外渗作用。由于神经肽的病理生理作用有赖于组织中肽神经纤维的存在，故该研究旨在通过对鼻息肉和正常鼻粘膜中三种神经肽的免疫组化比较研究探讨其分布类型及与鼻息肉发生的关系。取２０例鼻息肉…     

鼻变态反应中化学介质和鼻粘膜过度反应性对过度分泌的影响

伴随抗原抗体反应导致的化学介质释放,鼻粘膜过度反应性在鼻过敏症状的发生中起着主要作用。鼻粘膜过度反应性由两方面引起:①鼻粘膜感觉系统的敏感性增强;②与粘膜过敏无关的效应器官过度反应性。血管运动性鼻炎被认为足鼻粘膜副交感神经张力过高引起的,但是剧烈的鼻漏和鼻粘膜肿胀可以由于副交感神经末梢过多地释放乙酰胆碱引起,它继发于粘膜过敏所致的过多感觉冲动。本研究试图说明:①以下因素在多大程度上影响鼻变态反应的过度分泌作用,副交感神经末梢反射性     

蝶腭神经节电刺激对猫鼻粘膜神经末梢VIP释放的影响

为了解蝶腭神经节刺激对鼻粘膜神经肽释放的调节机制，用免疫组织细胞化学技术（ABC法）及放射免疫学方法观察电刺激蝶腭神经节对猫鼻粘膜神经末梢血管活性肠肽（vasoactiveintestinalpeptide，VIP）释放的影响。实验显示，蝶腭神经节刺激后，鼻粘膜静脉血浆VIP在15秒钟达高峰，随时间变化而逐渐下降。于此同时，分布于小动脉壁、小静脉壁、腺泡周围及上皮细胞间的VIP免疫反应阳性物质明显较神经节刺激前增多。实验结果表明蝶腭神经节刺激可促进猫鼻粘膜神经末梢VIP的释放。     

刺激自主神经鼻粘膜容量血管和阻力血管的反射性动态变化

本文报道电刺激猫的自主神经时对鼻粘膜容量血管和阻力血管的影响。容量血管的变化以体积描记球测定,阻力血管的变化以颌内动脉终支的血流阻力变化代表。刺激颈交感神经干时鼻粘膜容积减少,颌内动脉阻力增加,提示颈交感神经支配鼻粘膜的容量血管和阻力血管使其收缩。刺激迷走神经干时容量血管和阻力血管均扩张。刺激翼管神经,当电压为0.2～0.8伏时,鼻粘膜容量血管、阻力血管均扩张,提示翼管神经中包含的副交感神经发挥了     

神经反射在变应性鼻炎发病中的作用

变应性鼻炎发作时嗜酸性细胞释放的主要是碱性蛋白(MBP)损伤粘膜上皮,使感觉神经末梢暴露,组胺作用于暴露的神经末梢,使感觉神经产生动作电位,将组胺刺激传到中枢,经中枢整合后,经副交感神经传出至鼻粘膜,使鼻腺体分泌亢进、血管扩张;经有关神经传出至和呼吸有关的肌肉使之协同作用,产生喷嚏。因此认为神经反射在变应性鼻炎的发病中有重要作用。     

P物质对变应性鼻炎动物模型鼻粘膜上皮短路电流的影响

目的观察Ｐ物质（ＳＰ）作用于变应性鼻炎动物模型鼻粘膜引起的离子分泌改变导致的上皮表面短路电流（Ｓｈｏｒｔ－ｃｉｒｃｕｉｔｃｕｒｒｅｎｔ，Ｉｓｃ）的变化。方法以鸡蛋清蛋白致敏大鼠后，用Ｕｓｓ－ｉｎｇ室技术测定鼻粘膜上皮表面短路电流。并观察神经激肽受体（ＮＫ１）拮抗剂ＣＰ９６３４５、组胺Ｈ１受体拮抗剂吡拉明、Ｈ２受体拮抗剂雷尼替丁和河豚毒素对ＳＰ的阻断作用。结果经ＳＰ刺激，致敏大鼠鼻粘膜表面Ｉｓｃ显著增高。经四种物质预处理均能显著阻断ＳＰ引起的Ｉｓｃ变化。结论ＳＰ经感觉神经末梢释放后，可引起上皮表面离子电位变化、上皮通透性增高等一系列鼻粘膜病理变化。     

Vasomotor rhinitis--pathophysiological aspects.

Vasomotor rhinitis is commonly defined as an unspecific hyperractivity of the nasal mucosa. The symptoms might be due to increased parasympathetic activity to the nose with the release of vaso-secretory active substances. Experimental data from the cat suggest that the postganglionic parasympathetic mediator of nasal secretion is cholinergic, whereas the vascular responses appears to be due to a different mechanism. Apart from a rich sympathetic and parasympathetic innervation of the nasal mucosa there are other nerve fibres containing substance-P (SP) and vasoactive intestinal polypeptide (VIP). The secreto-vasomotor responses can be influenced by activation of these fibres and the atropine resistant vasodilatation seen following Vidian nerve stimulation thus may partly be due to activation and release of SP and VIP. Furthermore, other vasoactive substances released such as e.g. SRS or Kallikrein may participate in these reactions.     

Nasonasal reflex mechanisms in anaesthetized dogs.

In dogs anaesthetized with pentobarbitone, we recorded bilateral vascular and secretory responses to unilateral stimulation of intranasal afferent nerves. Nasonasal reflexes evoked by intranasal light mechanical stimulation, intranasal application of cold saline (2 ml at 3 degrees C), capsaicin (0.003-0.3 mmol) and antidromic electrical stimulation (15 V, 0.2 ms) of the trigeminal nerve at 10 Hz for 45 s were recorded. Vascular and secretory responses were studied before and after atropine pre-treatment, after ipsilateral section of the post-ganglionic parasympathetic fibres and the trigeminal nerve, and after administration of the ganglionic nicotinic receptor antagonist chlorisondamine. All stimuli studied induced bilateral increases in nasal arterial blood flow and secretion, although the contralateral responses were smaller under control conditions (p < 0.05). Bilateral vasodilatation evoked by mechanical stimulation, capsaicin and antidromic trigeminal nerve stimulation was resistant to atropine. The ipsilateral non-cholinergic vasodilatation evoked by mechanical stimulation or capsaicin was reduced by 50% (p < 0.05) after section of both trigeminal and post-ganglionic parasympathetic fibres. The remaining ipsilateral vasodilatation induced by these two stimuli was significantly reduced after chlorisondamine. The ipsilateral secretory responses to all stimuli studied were significantly reduced (p < 0.05), but not abolished by atropine. Contralateral secretory responses to all stimuli studied were not affected by atropine, the section of either the parasympathetic or trigeminal nerves, or chlorisondamine, suggesting the activation of local axon reflexes only. We conclude that unilateral intranasal stimulation of primary afferent neurons with light pressure, cold saline and capsaicin induces bilateral vascular and secretory responses via axon reflex mechanisms, as well as the activation of local and central sensory-parasympathetic reflex arcs.     

Origin and distribution of capsaicin-sensitive substance P-immunoreactive nerves in the nasal mucosa

In immunohistochemical studies, substance P-immunoreactivity (SP-IR) was found in a population of trigeminal ganglion cells in guinea pig, rat and cat. SP-IR nerve endings were found in the spinal trigeminal nucleus, around sphenopalatine ganglion cells, around blood vessels, as well as under and within the epithelium of the nasal mucosa. Ligation and denervation experiments in the cat indicated that the SP-IR nerves in the sphenopalatine ganglion and the nasal mucosa are of trigeminal origin. Capsaicin pretreatment of guinea pigs and rats resulted in a selective loss of the SP-IR nerves in the nasal mucosa and sphenopalatine ganglion, while the parasympathetic and sympathetic nerves were still present.     

The inhibition of norepinephrine release in nasal mucosa by acetylcholine

Tritiated norepinephrine was incorporated into isolated dog nasal mucosa. Electrical stimulation of this mucosa induced a release of the tritiated norepinephrine. Acetylcholine inhibited this release in a dose-related manner. The inhibition is prevented by atropine. This data provides further evidence for the existence of presynaptic, inhibitory, muscarinic receptors on the sympathetic nerve terminals in nasal blood vessels.     

Is the vidian nerve cholinergic?

Electrical stimulation of the parasympathetic nerve (vidian) to nasal mucosa induces a nasal secretion and a nasal vasodilation. We have provided additional evidence that, in the dog and cat, the secretory mechanism can be blocked with low doses of atropine sulfate (0.01 mg/kg), but the dilation mechanism is not blocked by high doses (1 mg/kg) of atropine sulfate. By some definitions therefore, the vasodilation is not a cholinergic effect. There appears to be a basic difference in the composition of the vidian nerve in the dog and cat. In the cat, the vidian appears to have a strong sympathetic component. In the dog it does not. The human vidian nerve, according to anatomists, is more like the dog's.     

Ruthenium red antagonism of capsaicin-induced vascular changes in the rat nasal mucosa

Mechanisms of capsaicin-induced vascular changes were examined in the nasal mucosa of anesthetized adult rats. Intra-arterial infusions of capsaicin at doses of 20–100 pmol/min into the external carotid artery resulted in a dose-dependent increase in nasal blood flow as assessed by laser-Doppler flowmetry. Intra-arterial infusion of ruthenium red (RR, 2.5–10 µmol) prior to the administration of capsaicin significantly inhibited the capsaicin-evoked response. The technique of vascular labelling was used to examine nasal mucosal vascular permeability. Intravenous administration of colloidal silver solution prior to capsaicin infusion resulted in accumulation of colloid in the walls of small blood vessels, indicative of enhanced vascular permeability. Vascular labelling was largely abolished after RR pretreatment. These findings suggest that neuropeptides released from trigeminal sensory nerve endings play a significant role in the local vascular and inflammatory reactions of the nasal mucosa. The experimental approach utilized in this study provides a promising model for defining the roles of capsaicin-sensitive afferent nerves in the mechanisms of allergic and/or inflammatory diseases affecting the nasal mucosa.     

Parasympathetic control of blood circulation and secretion in the nasal mucosa.

The effects of selective parasympathetic nerve activation on the secretory response and the vascular exchange and capacitance sections in the cat nasal mucosa were studied. The vascular events were investigated by measuring the local disappearnce of 125I- and changes in gross pulse rate from 131I- labelled serum albumin as monitored over the nose. A frequency-dependent increase in nasal secretion and local blood content occurred in the range 0.5-12 imp/sec: an increase in disappearance rate was observed at the same time. This indicates that the vascular and secretory responses are activated simultaneously. The secretory responses, but not the vascular events, were shown to be blocked by atropine. The results thus shown that the postganglionic parasympathetic mediator of nasal secretion is cholinergic, whereas the vasodilatation appears to be due to a different mechanism, which is not sensitieve to atropine. The beneficial effect of some antihistamines in vasomotor rhinitis may thus be due to their anticholinergic properties.     

Sensitive innervation of the nasal mucosa: current concepts

Sensitive innervation of the nasal fossae by the trigeminal nerves is not a simple passive system of information transmission, but also plays a considerable role in nasal physiology. An antidromic transmission mechanism is in fact added to the conventional centripetal transmission, leading to the release of neurotransmitters (P-substance and C.G.R.P.) at the level of the neuronasal nerve endings. These substances can cause inflammation and vasodilatation (sub-mucosal and perivascular) in certain sites of the 5th nerve, and stimulate the second parasympathetic neurone at the level of the sphenopalatine ganglion. Such phenomena, when they extend beyond physiology, can be the source of local pathology (rhinitis) or loco-regional pathology (headaches).