Garrity E R, Stimler N P, Munoz N M, Fried R, Leff A R
J Appl Physiol Respir Environ Exerc Physiol. 1983 Dec;55(6):1803-10. doi: 10.1152/jappl.1983.55.6.1803.
We studied the response of bronchial smooth muscle to mast cell degranulation with Ascaris suum antigen (AA) and compound 48/80 (48/80) in 26 mongrel dogs in situ. Bronchial smooth muscle response was measured isometrically in situ from a segment of the right middle lobe bronchus; tracheal response was monitored isometrically as a control. After intra-arterial (ia) injection of AA into the bronchial circulation, bronchial contraction preceded tracheal contraction by 19.2 +/- 4.6 s (P less than 0.002). Bronchial contraction to AA (21.7 +/- 3.4 g) was substantially greater than to 48/80 (10.5 +/- 1.8 g, P less than 0.05) corresponding to differences in maximal systemic histamine concentrations (146 +/- 24.1 vs. 1000 +/- 236 ng/ml, P less than 0.01). In 5 dogs, the effect of leukotriene D4 (LTD4) and FPL 55712 was studied. Injection of 10(-8) mol ia LTD4 caused no bronchial contraction. In four dogs, 10(-7) mol FPL 55712 caused no bronchial relaxation after initial precontraction during immune degranulation with AA; intravenous chlorpheniramine (5 mg/kg) caused 69.7 +/- 9.4% relaxation. We demonstrate a model that permits selective immune degranulation of a single major resistance bronchus in situ. We conclude that AA-induced degranulation in dogs caused bronchial contraction predominantly by secretion of preformed mediator.
我们在26只杂种犬体内研究了支气管平滑肌对猪蛔虫抗原(AA)和化合物48/80(48/80)诱导的肥大细胞脱颗粒的反应。在原位等长测量右中叶支气管一段的支气管平滑肌反应;等长监测气管反应作为对照。经动脉内(ia)将AA注入支气管循环后,支气管收缩比气管收缩提前19.2±4.6秒(P<0.002)。支气管对AA的收缩(21.7±3.4克)明显大于对48/80的收缩(10.5±1.8克,P<0.05),这与最大全身组胺浓度的差异相对应(146±24.1对1000±236纳克/毫升,P<0.01)。在5只犬中,研究了白三烯D4(LTD4)和FPL 55712的作用。注入10^(-8)摩尔ia LTD4未引起支气管收缩。在4只犬中,在AA免疫脱颗粒初始预收缩后,注入10^(-7)摩尔FPL 55712未引起支气管舒张;静脉注射氯苯那敏(5毫克/千克)引起69.7±9.4%的舒张。我们展示了一个能在原位对单个主要阻力支气管进行选择性免疫脱颗粒的模型。我们得出结论,犬体内AA诱导的脱颗粒主要通过预先形成的介质分泌导致支气管收缩。