Ben-Harari R R, Tagliente T M
Department of Anesthesiology, NYU Medical Center, NY 10016.
Life Sci. 1991;49(12):907-13. doi: 10.1016/0024-3205(91)90176-c.
An alteration in the handling of Ca2+ has been proposed as the pathogenic mechanism underlying the airway smooth muscle hyperresponsiveness of asthma. The present study tested the hypothesis that the altered responsiveness of receptor operated contraction to carbachol in allergic asthma results from a change in the phasic or tonic components. Using a kinetic approach, the phasic and tonic responses to 10 microM carbachol were quantitated in isolated epithelium-free trachea 21 days after guinea-pigs were sensitized with ovalbumin and aluminum hydroxide (as adjuvant) to generate preferentially IgE-like antibodies. Sensitization was confirmed by challenge of the isolated trachea with ovalbumin. The steady-state and kinetic characteristics of the phasic and tonic responses were the same from sensitized animals and animals treated with saline and aluminum hydroxide (control) and before and after challenge of the trachea from both groups of animals. The present results demonstrate that immunologic sensitization and challenge do not appear to elicit a defect in the phasic or tonic responses of receptor mediated contractions in airway smooth muscle and suggest there is no alteration in the handling of Ca2+ in smooth muscle from sensitized and challenged guinea-pig trachea.
钙（Ca2+）处理的改变被认为是哮喘气道平滑肌高反应性的潜在致病机制。本研究检验了如下假设：过敏性哮喘中受体介导的对卡巴胆碱收缩反应性的改变是由相位或张力成分的变化引起的。采用动力学方法，在豚鼠用卵清蛋白和氢氧化铝（作为佐剂）致敏以优先产生IgE样抗体21天后，对离体无上皮气管对10微摩尔卡巴胆碱的相位和张力反应进行定量。通过用卵清蛋白刺激离体气管来确认致敏情况。致敏动物、用盐水和氢氧化铝处理的动物（对照）以及两组动物气管刺激前后，相位和张力反应的稳态及动力学特征均相同。目前的结果表明，免疫致敏和刺激似乎并未引发气道平滑肌中受体介导收缩的相位或张力反应缺陷，提示致敏和受刺激的豚鼠气管平滑肌中钙（Ca2+）处理没有改变。
