González R, García M, de la Vega A R, Arruzazabala M L, Pérez H
Allergol Immunopathol (Madr). 1979 Mar-Apr;7(2):125-34.
Diethylcarbamazine citrate (DEC) is an anthelmintic drug which has been used recently, with varying results, in the treatment of bronchial asthma. We have examined the pharmacological activity of this drug in several in vivo and in vitro models of experimental anaphylaxis. DEC at doses of 25 and 50 mg per kg given intraperitoneally significantly reduced the mortality rate in sensitized guinea pigs during protracted shock phase but did not modify the time for the appearance of dyspnoea when antigen (egg albumin) was administered as aerosol. Nor did DEC at therapeutic doses inhibit the degranulation and histamine release from rat isolated peritoneal mast cells induced by phospholipase A, compound 48/80, and antigen respectively. It has been suggested that one possible explanation for the apparent effectiveness of DEC in asthma is its ability to antagonize prostaglandin F2 alpha. Our results using in vivo and in vitro models of bronchoconstriction in guinea pigs do not support this hypothesis to explain the inhibition of protacted shock by DEC.
枸橼酸乙胺嗪（DEC）是一种驱虫药，最近已用于治疗支气管哮喘，但其疗效各异。我们在几种实验性过敏反应的体内和体外模型中研究了该药物的药理活性。腹腔注射剂量为每公斤25毫克和50毫克的DEC可显著降低致敏豚鼠在延长休克期的死亡率，但当以气雾剂形式给予抗原（卵清蛋白）时，并未改变呼吸困难出现的时间。治疗剂量的DEC也不能抑制磷脂酶A、化合物48/80和抗原分别诱导的大鼠离体腹膜肥大细胞的脱颗粒和组胺释放。有人提出，DEC在哮喘中明显有效的一个可能解释是其拮抗前列腺素F2α的能力。我们使用豚鼠支气管收缩的体内和体外模型所得到的结果并不支持这一假设来解释DEC对延长休克的抑制作用。
