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白三烯C4和水肿在豚鼠急性过敏性支气管收缩中的作用。

Role of leukotriene C4 and edema in the acute allergic bronchoconstriction in the guinea pig.

作者信息

Vargas M H, Selman M, Campos G, Montaño L M

机构信息

Unidad de Inv. Inst. Nal. de Enfermedades Respiratorias, S.S., México, D.F.

出版信息

Arch Invest Med (Mex). 1991 Apr-Jun;22(2):143-9.

PMID:1819989
Abstract

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.

摘要

体外研究表明白三烯参与急性过敏性支气管收缩,尽管这一点在体内研究中尚未得到明确证实。另一方面,抗原激发过程中产生的水肿可能是促成这种支气管收缩的另一个因素。在本研究中,我们对免疫的豚鼠静脉注射1mg/kg卵清蛋白(OA)诱导过敏性支气管收缩期间支气管肺泡灌洗中的免疫反应性白三烯C4(iLTC4)浓度进行了定量,同时也对在这种支气管收缩之前和期间获得的豚鼠肺组织碎片中的含水量进行了测定。我们发现,在支气管收缩反应的2、5和10分钟时(中位数分别为1.10、0.29和1.37 ng/ml),iLTC4的基础浓度(中位数为1.06 ng/ml)没有显著变化。在未免疫的豚鼠、免疫的豚鼠以及支气管收缩15分钟时,肺组织碎片中的含水量没有变化(平均值±标准误分别为79.32%±0.18、79.10%±0.31和79.13%±0.40%)。此外,异丙肾上腺素(20μg/kg,静脉注射)能迅速逆转较高抗原剂量(OA,3.1mg/kg静脉注射)诱导的约70%的支气管收缩;残余梗阻与肺组织碎片中含水量增加无关(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并非由于iLTC4释放增加或水肿产生,气道平滑肌收缩是该反应的主要组成部分。

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