Chand N, Diamantis W, Sofia R D
Br J Pharmacol. 1987 May;91(1):17-22. doi: 10.1111/j.1476-5381.1987.tb08978.x.
The effect of antigen challenge on cold provocation (30-10 degrees C) in isolated tracheal segments from control (normal) and ovalbumin-sensitized rats was studied. Sensitization alone or acute cold provocation (10 degrees C) alone was not sufficient to cause contraction of tracheal smooth muscle preparation. Following recovery from antigen-induced responses (Schultz-Dale phenomenon) in sensitized rat segments, cold provocation induced strong contractile responses. Both the antigen-induced contractions and the subsequent development of airway hyperreactivity to cold were dependent on extracellular Ca2+ and inhibited by verapamil. The data in this study indicate that extracellular Ca2+ plays an obligatory role in the mediation of antigen-induced contractile responses as well as the subsequent development of hyperreactivity to cold provocation in rat tracheal smooth muscle.
研究了抗原激发对来自对照(正常)大鼠和卵清蛋白致敏大鼠的离体气管段冷激发(30 - 10摄氏度)的影响。单独致敏或单独急性冷激发(10摄氏度)不足以引起气管平滑肌标本收缩。在致敏大鼠气管段从抗原诱导的反应(舒尔茨 - 戴尔现象)恢复后,冷激发诱导强烈的收缩反应。抗原诱导的收缩以及随后气道对冷的高反应性的发展均依赖于细胞外Ca2 +,并被维拉帕米抑制。本研究数据表明,细胞外Ca2 +在介导抗原诱导的收缩反应以及随后大鼠气管平滑肌对冷激发的高反应性发展中起重要作用。