Pretolani M, Page C P, Lefort J, Lagente V, Vargaftig B B
Eur J Pharmacol. 1986 Jun 24;125(3):403-9. doi: 10.1016/0014-2999(86)90796-x.
The intrathoracic accumulation of radiolabelled platelets was recorded in anaesthesized, sensitized guinea-pigs concomitantly with changes in airways resistance during active anaphylaxis. Antigen challenge induced an increased airway resistance associated with intrathoracic platelet accumulation, thrombocytopenia and leukopenia. Bronchoconstriction, but not the haematological changes, was modified by a combination of mepyramine, methysergide and aspirin. The addition of FPL 55712 and PGI2 to this cocktail of drugs additionally inhibited the thrombocytopenia and leukopenia but not the intrathoracic accumulation of platelets induced by antigen challenge. PGI2 was alone able to significantly inhibit the intrathoracic platelet accumulation, but not the bronchoconstriction induced by antigen challenge. These results suggest that active anaphylaxis is associated with activation of blood elements and subsequent pulmonary entrapment of platelets but that the platelet release reaction rather than the embolisation of platelet aggregates is the critical step in the induction of allergic bronchoconstriction in the guinea-pig.
在麻醉的致敏豚鼠中记录放射性标记血小板的胸腔内积聚情况，并同时观察主动过敏反应期间气道阻力的变化。抗原激发导致气道阻力增加，同时伴有胸腔内血小板积聚、血小板减少和白细胞减少。美吡拉敏、甲基麦角新碱和阿司匹林联合使用可改善支气管收缩，但对血液学变化无影响。在这种药物组合中加入FPL 55712和前列环素（PGI2）可进一步抑制血小板减少和白细胞减少，但不能抑制抗原激发诱导的胸腔内血小板积聚。单独使用PGI2能够显著抑制胸腔内血小板积聚，但不能抑制抗原激发诱导的支气管收缩。这些结果表明，主动过敏反应与血液成分的激活以及随后血小板在肺部的滞留有关，但血小板释放反应而非血小板聚集体的栓塞是诱导豚鼠过敏性支气管收缩的关键步骤。
