Sympathetic modulation of biochemical and physiological response to immune degranulation in canine bronchial airways in vivo.
Sympathetic modulation of biochemical and physiological response to immune degranulation in canine bronchial airways in vivo.
复制标题
体内犬支气管气道对免疫脱颗粒的生化和生理反应的交感调节。
DOI：
10.1172/jci111923
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Leff,AR
中科院分区：
文献类型：
--
作者：
Garrity,ER;Stimler,NP;Munoz,NM;Tallet,J;David,AC;Leff,AR
研究了交感神经刺激对猪蛔虫抗原对肥大细胞脱粒后支气管平滑肌收缩反应的影响。等距测量单个右中叶支气管的支气管平滑肌反应。通过支气管动脉循环给药一剂量引起介质最大释放的抗原。在动脉内（i.a）给药后，每隔15 s测定血浆组胺浓度。同时从右心和股动脉取血，测定肥大细胞脱颗粒过程中支气管组胺浓度的动静脉差异（AVd）。在9只出现支气管肥大细胞脱肉芽的犬中，支气管平滑肌收缩量为22.3 +/- 2.95 g，支气管组胺浓度平均AVd为188 +/- 41.5 ng/ml。另外6只静脉注射0.75 ~ 1.0 mg/kg阿托品阻断毒虫碱的狗，在静脉注射1,1-二甲基-4-苯基哌嗪碘化（DMPP）稳定刺激1分钟后给予a抗原。在猪蛔虫抗原刺激过程中，交感神经刺激可完全抑制支气管平滑肌对ia抗原的收缩反应（P < 0.001），且未检测到支气管组胺浓度的显著AVd （9.8 +/- 16.0 ng/ml，与对照组相比P < 0.01）。对照组血浆组胺浓度峰值为1138 +/- 237 ng/ml，交感神经刺激组为310 +/- 135 ng/ml （P < 0.01）。在4只对静脉注射抗原进行全身性过敏反应的狗中，随后用静脉注射DMPP刺激交感神经使支气管运动性张力降低到基线对照的约70%。外源性诱导的交感神经刺激可显著抑制过敏犬对猪蛔虫抗原的全身肥大细胞脱颗粒。交感神经系统的最大刺激引起呼吸肥大细胞分泌组胺和支气管平滑肌对循环介质收缩的实质性抑制。图片
The effect of sympathetic stimulation on bronchial smooth muscle contractile response after mast cell degranulation with Ascaris suum antigen was studied in 36 natively allergic dogs in situ. Bronchial smooth muscle response was measured isometrically in a single right middle lobe bronchus. A dose of antigen causing maximal release of mediator was administered to the bronchus through the bronchial arterial circulation. Serial plasma histamine concentrations were determined at 15-s intervals after intra-arterial (i.a.) administration of antigen. Samples of blood were obtained simultaneously from right heart and femoral artery, and arteriovenous difference (AVd) in histamine concentration across the bronchus was determined during mast cell degranulation. In nine dogs showing bronchial mast cell degranulation to antigen challenge, bronchial smooth muscle contraction was 22.3 +/- 2.95 g and the mean AVd in histamine concentration across the bronchus was 188 +/- 41.5 ng/ml. Six other dogs having muscarinic blockade with 0.75-1.0 mg/kg intravenous atropine were given i.a. antigen after 1 min of steady-state sympathetic stimulation with intravenous 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP). Sympathetic stimulation during Ascaris suum antigen challenge caused complete inhibition of bronchial smooth muscle contractile response to i.a. antigen (P less than 0.001), and a significant AVd in histamine concentration across the bronchus (9.8 +/- 16.0 ng/ml; P less than 0.01 vs. control) was not detected. Peak plasma histamine concentration in control dogs was 1,138 +/- 237 ng/ml vs. 310 +/- 135 ng/ml in animals receiving sympathetic stimulation (P less than 0.01). In four dogs undergoing systemic anaphylaxis to i.v. antigen, subsequent sympathetic stimulation with i.v. DMPP reduced bronchomotor tone to approximately 70% of base-line control. Exogenously induced sympathetic stimulation can substantially inhibit systemic mast cell degranulation to Ascaris suum antigen in allergic dogs. Maximal stimulation of the sympathetic nervous system causes substantial inhibition of respiratory mast cell secretion of histamine and bronchial smooth muscle contraction to circulating mediator.Images