Neurogenic inflammation. A model for studying efferent actions of sensory nerves.
Neurogenic inflammation. A model for studying efferent actions of sensory nerves.
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发表时间：
1996
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通讯作者：
D. M. McDonald;Jeffrey J. Bowden;P. Baluk;N. Bunnett
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作者：
D. M. McDonald;Jeffrey J. Bowden;P. Baluk;N. Bunnett
一些证据表明，颈动脉小体的感觉神经除了向大脑传导化学感受性冲动的传入功能外，还具有传出功能。然而，很难将感觉神经末梢释放的物质记录在球体细胞上，也很难确定这种传出功能是否在化学接收中发挥作用。相比之下，神经源性炎症现象在大鼠和豚鼠身上相对容易研究，并已被证明是分析感觉神经传出行为的一个信息模型系统。神经源性炎症的主要特征是血浆渗漏。化学刺激物激活无髓感觉神经，通过触发感觉神经纤维释放物质，导致皮肤、呼吸道和其他器官的血浆渗漏。由一些感觉神经元合成和释放的P物质似乎是主要的活性介质，其他速激肽、降钙素基因相关肽，可能还有其他多肽也参与了这一过程。神经源性炎症是P物质作用于NK1受体的结果，选择性NK1受体激动剂和拮抗剂证实了这一点。参与血浆渗漏的NK1受体位于毛细血管后小静脉和集合小静脉的内皮细胞上。在P物质激活NK1受体的几秒钟内，靶血管内皮细胞就形成了缝隙。内皮间隙是暂时的，泄漏通常在几分钟内就会结束。然而，在大鼠肺支原体感染等病理条件下，这种反应的幅度会增加，从而导致慢性呼吸道炎症性疾病。感染的呼吸道粘膜由于血管生成而形成异常的血管，新生血管的内皮细胞表达NK1受体的数量增加，因此对P物质异常敏感。对神经源性炎症的研究不仅有助于了解感觉神经的传出活动，而且有助于深入了解内皮细胞和随后的血浆渗漏的炎症变化的机制和后果。
Several lines of evidence suggest that sensory nerves of the carotid body have an efferent function in addition to their afferent function of conducting chemoreceptive impulses to the brain. However, it has been difficult to document the release of substances from sensory nerve terminals on glomus cells and to determine whether such an efferent function plays a role in chemoreception. By comparison, the phenomenon of neurogenic inflammation has been relatively easy to study in rats and guinea pigs and has proven to be an informative model system for analyzing efferent actions of sensory nerves. The main characteristic of neurogenic inflammation is plasma leakage. Chemical irritants that activate unmyelinated sensory nerves cause plasma leakage in the skin, respiratory tract, and other organs by triggering the release of substances from sensory nerve fibers. Substance P, which is synthesized and released by some sensory neurons, appears to be the main active mediator, although other tachykinins, calcitonin gene-related peptide, and perhaps other peptides may also participate. Neurogenic inflammation results from the action of substance P on NK1 receptors, as demonstrated by selective NK1 receptor agonists and antagonists. The NK1 receptors involved in plasma leakage are located on the endothelial cells of postcapillary venules and collecting venules. Within seconds of the activation of NK1 receptors by substance P, gaps form in the endothelium of target vessels. The endothelial gaps are transient, and the leak normally ends in a few minutes. However, the magnitude of the response can increase in pathological conditions such as Mycoplasma pulmonis infection in rats, which results in a chronic inflammatory disease of the respiratory tract. The infected airway mucosa becomes abnormally vascular as a result of angiogenesis, and the endothelial cells of the newly formed vessels express increased numbers of NK1 receptors and thus are abnormally sensitive to substance P. Studies of neurogenic inflammation not only have helped to understand the efferent actions of sensory nerves but also have given insight into the mechanism and consequences of inflammatory changes in endothelial cells and in the plasma leakage that follows.