白三烯C4和水肿在豚鼠急性变应性支气管收缩中的作用。

Archivos de investigacion medica Pub Date : 1991-04-01
M H Vargas, M Selman, G Campos, L M Montaño
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引用次数: 0

摘要

体外研究表明,白三烯与急性过敏性支气管收缩有关,尽管这在体内研究中尚未得到明确证实。另一方面,在抗原性刺激过程中产生的水肿可能是有利于这种支气管收缩的另一个因素。在本工作中,我们量化了免疫豚鼠在1 mg/kg卵白蛋白(OA)诱导的过敏性支气管收缩期间,支气管肺泡灌洗液中免疫反应性白三烯C4 (iLTC4)的浓度,以及在支气管收缩之前和期间获得的豚鼠肺片段的水含量。我们发现,在支气管收缩反应的2、5和10分钟(分别为1.10、0.29和1.37 ng/ml)时,iLTC4的基础浓度(中位数为1.06 ng/ml)没有显著改变。未免疫豚鼠、免疫豚鼠和支气管收缩15 min时肺碎片含水量没有变化(平均+/- SEM分别为79.32% +/- 0.18、79.10% +/- 0.31和79.13% +/- 0.40%)。此外,异丙肾上腺素(20微克/公斤,静脉注射)能迅速恢复高抗原剂量(OA, 3.1毫克/公斤静脉注射)引起的约70%的支气管收缩;残余梗阻与肺碎片含水量增加无关(78.13% +/- 0.43)。这些结果表明,在该模型中,急性过敏性支气管收缩不是由于iLTC4释放增加或水肿产生,气道平滑肌收缩是这种反应的主要组成部分。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of leukotriene C4 and edema in the acute allergic bronchoconstriction in the guinea pig.

In vitro studies have suggested that leukotrienes are involved in acute allergic bronchoconstriction, though this has not been definitively corroborated yet in in vivo studies. On the other hand, edema production during antigenic challenge could be an additional factor favouring such bronchoconstriction. In the present work we quantified immunoreactive leukotriene C4 (iLTC4) concentrations in bronchoalveolar lavages during allergic bronchoconstriction induced by 1 mg/kg i.v. ovalbumin (OA) in immunized guinea pigs, as well as water content in guinea pig lung fragments obtained before and during this bronchoconstriction. We found that basal concentrations of iLTC4 (median 1.06 ng/ml) were not significantly modified at 2, 5 and 10 min (median 1.10, 0.29 and 1.37 ng/ml, respectively) of the bronchoconstrictor response. Water content in lung fragments did not change among non-immunized guinea pigs, immunized ones and at 15 min of bronchoconstriction (mean +/- SEM 79.32% +/- 0.18, 79.10% +/- 0.31 and 79.13% +/- 0.40%, respectively). In addition, isoproterenol (20 micrograms/kg, i.v.) rapidly reverted about 70% of the bronchoconstriction induced by a higher antigenic dose (OA, 3.1 mg/kg i.v.); residual obstruction was not associated with increased water content in lung fragments (78.13% +/- 0.43). These results suggest that in this model, acute allergic bronchoconstriction is not due to an increased iLTC4 release or to edema production, and that airway smooth muscle contraction is the main component of this response.

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