白三烯抑制剂不能阻断犬的低氧性肺血管收缩。

Leukotriene inhibitors do not block hypoxic pulmonary vasoconstriction in dogs.

作者信息

Schuster D P, Dennis D R

出版信息

J Appl Physiol (1985). 1987 May;62(5):1808-13. doi: 10.1152/jappl.1987.62.5.1808.

DOI:10.1152/jappl.1987.62.5.1808

Abstract

We studied whether intravenously administered inhibitors of leukotriene synthesis (diethylcarbamazine, DEC) or end-organ effect (FPL-55712) would change the distribution of regional pulmonary blood flow (rPBF) caused by left lower lobe (LLL) alveolar hypoxia in dogs. Both drugs failed to alter rPBF. In addition, the pressor response to whole-lung hypoxia was not blocked by an FPL-55712 infusion. On the other hand, nitroprusside, as a nonspecific vasodilator also administered intravenously, was able to partially reverse the effects of LLL hypoxia on rPBF. Thus our data do not support a role for leukotriene mediation of hypoxic pulmonary vasoconstriction in dogs.

摘要

我们研究了静脉注射白三烯合成抑制剂（乙胺嗪，DEC）或终末器官效应抑制剂（FPL - 55712）是否会改变犬左下叶（LLL）肺泡缺氧引起的局部肺血流（rPBF）分布。两种药物均未能改变rPBF。此外，FPL - 55712输注并未阻断对全肺缺氧的升压反应。另一方面，作为同样静脉注射的非特异性血管扩张剂，硝普钠能够部分逆转LLL缺氧对rPBF的影响。因此，我们的数据不支持白三烯在犬低氧性肺血管收缩中起介导作用。