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Leukotriene inhibitors do not block hypoxic pulmonary vasoconstriction in dogs.

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.
AuthorsD P Schuster, D R Dennis
JournalJournal of applied physiology (Bethesda, Md. : 1985) (J Appl Physiol (1985)) Vol. 62 Issue 5 Pg. 1808-13 (May 1987) ISSN: 8750-7587 [Print] United States
PMID3597254 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Chromones
  • SRS-A
  • Nitroprusside
  • FPL 55712
  • Diethylcarbamazine
Topics
  • Animals
  • Chromones (pharmacology)
  • Diethylcarbamazine (pharmacology)
  • Dogs
  • Hypoxia (drug therapy, physiopathology)
  • Nitroprusside (pharmacology)
  • Pulmonary Alveoli (blood supply, physiopathology)
  • Pulmonary Circulation (drug effects)
  • SRS-A (antagonists & inhibitors, biosynthesis)
  • Vasoconstriction (drug effects)

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