ET-1 induced bronchoconstriction in the early phase but not late phase of anesthetized dogs is inhibited by indomethacin and ICI 198615

Biochem Biophys Res Commun. 1992 Mar 31;183(3):1197-202. doi: 10.1016/s0006-291x(05)80317-1.

Abstract

Intratracheally injected or aerosolized ET-1 induced quick and long-lasting bronchoconstriction of anesthetized mongrel dogs, thus increasing respiratory resistance(Rrs) with concomitantly decreasing dynamic compliance(Cdyn). As collateral resistance(Rcs) was measured postexposure to aerosolized ET-1 using wedged bronchoscope technique, ET-1 increased Rcs in a dose and time dependent manner. The increase attained maximal in 2 min and then, gradually declined. When the dogs were pretreated with the intravenous injection of 0.1 micrograms/kg ICI 198615, an inhibitor of lipoxygenase, the constrictive response was slowed down. Essentially similar results were also observed with the intravenous injection of 5 mg/kg indomethacin. Our observations suggest that the early phase of the ET-1 induced bronchoconstriction is mediated by eicosanoid metabolites.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Anesthesia, Intravenous*
  • Animals
  • Bronchoconstriction / drug effects
  • Bronchoconstriction / physiology*
  • Dogs
  • Dose-Response Relationship, Drug
  • Endothelins / pharmacology*
  • Indazoles / pharmacology*
  • Indomethacin / pharmacology*
  • SRS-A / antagonists & inhibitors

Substances

  • Endothelins
  • Indazoles
  • SRS-A
  • ICI 198615
  • Indomethacin