Gjerde E A, Woie K, Reed R K
Department of Physiology, University of Bergen, Norway.
Acta Physiol Scand. 1997 Nov;161(3):411-8. doi: 10.1046/j.1365-201X.1997.00231.x.
Neurogenic inflammation is mediated by neuropeptides released from sensory nerves following electrical stimulation of the vagal nerve or by capsaicin. The released neuropeptides are, among others, calcitonin gene-related peptide and substance P, which both induce vasodilation, while only substance P induces plasma extravasation. Electrical stimulation of the vagal nerve induces increased negativity of interstitial fluid pressure (Pif), which will contribute to enhance oedema formation. Pif was measured, on the abluminal side of the surgically exposed trachea, with sharpened glass capillaries (4-10 microns) connected to a servo-controlled counterpressure system. Measurements were performed after circulatory arrest, since the oedema formation associated with acute inflammation will increase Pif in a positive direction, which may potentially underestimate the increased negativity of Pif. Experiments were carried out in pentobarbital anaesthetized (50 mg kg-1) Wistar-Møller rats. Pif in control rats averaged -1.2 +/- 0.9 (SD) mmHg (n = 9). Intravenous injection of capsaicin (65.0 nmol) and calcitonin gene-related peptide (1.3 nmol) increased the negativity of Pif to -4.0 +/- 1.2 mmHg (n = 8) (P < 0.01) and -4.7 +/- 2.0 mmHg (n = 9) (P < 0.01), respectively. Intravenous injection of substance P (7.4 nmol, n = 9; and 37.0 nmol, n = 8) did not affect Pif compared to control (P > 0.05). Similarly, potentiation of the available substance P with thiorphan or captopril did not increase the negative Pif, nor did injection of stable substance P analogues. Thus, the present study seems to support the theory that, in rat trachea, the increased negativity of Pif after intravenous injection of capsaicin and after vagal stimulation is caused by calcitonin gene-related peptide.
神经源性炎症是由迷走神经电刺激或辣椒素刺激后感觉神经释放的神经肽介导的。释放的神经肽包括降钙素基因相关肽和P物质等，二者均可诱导血管舒张，而只有P物质可诱导血浆外渗。迷走神经电刺激可导致组织间液压力（Pif）负值增加，这将促进水肿形成。在手术暴露的气管腔外侧面，使用连接到伺服控制反压系统的尖锐玻璃毛细管（4 - 10微米）测量Pif。测量在循环停止后进行，因为与急性炎症相关的水肿形成会使Pif正向增加，这可能会低估Pif增加的负值。实验在戊巴比妥麻醉（50 mg/kg）的Wistar - Møller大鼠中进行。对照大鼠的Pif平均为 - 1.2±0.9（标准差）mmHg（n = 9）。静脉注射辣椒素（65.0 nmol）和降钙素基因相关肽（1.3 nmol）分别使Pif的负值增加到 - 4.0±1.2 mmHg（n = 8）（P < 0.01）和 - 4.7±2.0 mmHg（n = 9）（P < 0.01）。与对照相比，静脉注射P物质（7.4 nmol，n = 9；和37.0 nmol，n = 8）对Pif无影响（P > 0.05）。同样，用硫喷妥或卡托普利增强可用的P物质也不会增加Pif的负值，注射稳定的P物质类似物也不会。因此，本研究似乎支持这样一种理论，即在大鼠气管中，静脉注射辣椒素和迷走神经刺激后Pif负值增加是由降钙素基因相关肽引起的。
