Widdicombe J G
Department of Physiology, St. George's Hospital Medical School, London, United Kingdom.
Am Rev Respir Dis. 1991 Mar;143(3 Pt 2):S18-21. doi: 10.1164/ajrccm/143.3_Pt_2.S18.
The tracheobronchial vasculature is controlled by adrenergic, cholinergic, and peptidergic nervous mechanisms. Sympathetic nerves release norepinephrine and neuropeptide Y (NPY), which are both constrictor agents, the latter being long-lasting. Parasympathetic nerves release acetylcholine and usually vasoactive intestinal polypeptide (VIP), both of which are vasodilators, VIP being the longer lasting. These motor nerves are controlled by many reflex inputs. Activation of pulmonary C-fiber receptors by irritants and inflammatory mediators causes a powerful vasodilatation, mainly via sympathetic motor nerves. Cardiac and chemoreceptor reflexes also influence airway vascular tone. Sensory nerves in the airway mucosa are responsible for local axon reflexes in response to irritants and inflammatory mediators. These nerves contain neuropeptides such as substance P (SP), neurokinins A and B (NKA, NKB), and calcitonin gene-related peptide (CGRP). All these neuropeptides are powerful vasodilators. Thus, inflammatory conditions in the lungs such as asthma cause vasodilation by local direct action of mediators, by axon reflexes, and by central nervous reflexes. The vasodilation could lead to mucosal edema. Thus, airway vascular responses have to be added to bronchoconstriction and mucus secretion as part of the mucosal pathology of asthma.
气管支气管血管系统受肾上腺素能、胆碱能和肽能神经机制控制。交感神经释放去甲肾上腺素和神经肽Y（NPY），二者均为血管收缩剂，后者作用持久。副交感神经释放乙酰胆碱，通常还释放血管活性肠肽（VIP），二者均为血管扩张剂，VIP作用更持久。这些运动神经受多种反射性传入控制。刺激物和炎症介质激活肺C纤维感受器，主要通过交感运动神经引起强烈的血管扩张。心脏和化学感受器反射也影响气道血管张力。气道黏膜中的感觉神经负责对刺激物和炎症介质产生局部轴突反射。这些神经含有诸如P物质（SP）、神经激肽A和B（NKA、NKB）以及降钙素基因相关肽（CGRP）等神经肽。所有这些神经肽都是强大的血管扩张剂。因此，肺部的炎症状态如哮喘可通过介质的局部直接作用、轴突反射和中枢神经反射引起血管扩张。血管扩张可导致黏膜水肿。因此，气道血管反应必须作为哮喘黏膜病理的一部分，与支气管收缩和黏液分泌一并考虑。
