Microsphere-induced bronchial artery vasodilation: Role of adenosine, prostacyclin, and nitric oxide

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Abstract

We previously found that injection of 15-μm microspheres into the bronchial artery of sheep decreased bronchial artery resistance. This effect was inhibited partially by indomethacin or 8-phenyltheophylline, suggesting that microspheres caused release of a dilating prostaglandin and adenosine. To identify the prostaglandin and confirm adenosine release, we perfused the bronchial artery in anesthetized sheep. In 12 sheep, bronchial artery blood samples were obtained before and after the infusion of 1 x 106 microspheres or microsphere diluent into the bronchial artery. Microspheres, but not diluent, decreased bronchial artery resistance by 40% and increased bronchial artery plasma 6-ketoprostaglandin F(1α) (194.7 ± 45.0 to 496.5 ± 101.3 pg/ml), the stable metabolite of prostacyclin, and prostaglandin (PG) F(2α) (28.1 ± 4.4 to 46.2 ± 9.7 pg/ml). There were n changes in PGD2, PGE2, thromboxane B2, adenosine, inosine, or hypoxanthine. Pretreatment with dipyridamole, an adenosine uptake inhibitor, did not affect bronchial artery nucleoside concentrations (n = 7). Microsphere-induced vasodilation was not enhanced by dipyridamole (n = 9) and was not inhibited by either the adenosine receptor antagonist xanthine amine congener (n = 4) or the nitric oxide (NO) synthase inhibitor N(G)-monomethyl-L-arginine (n = 8). These results do not support a role for either adenosine or NO and suggest that microspheres caused bronchial artery vasodilation through release of prostacylin and an unidentified vasodilator.

Original languageEnglish (US)
Pages (from-to)H760-H768
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume274
Issue number3 43-3
DOIs
StatePublished - Mar 1998

Keywords

  • Indomethacin
  • N(G)-monomethyl-L-arginine
  • Sheep
  • Xanthine amine congener

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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