Effects of cigarette smoking, hypoxia and vasoactive mediators on the production of PGI2 and TXA2 in cultured pulmonary artery endothelial cells

Su Yun-chao, Wang Di-xun

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Effects of cigarette smoke extract (CSE) and some vasoactive mediators on the production of PGI2 and TXA2 in normoxic and hypoxic pulmonary artery endothelial cells (PAECs) in culture were studied. The production of PGI2 in PAECs was inhibited by hypoxia or verapamil, but promoted by angiotensin II (A II), noradrenaline (NE) or platelet activating factor (PAF), while that of TXA2 slightly increased except when treated with PAF. The effect of A II, NE, PAF and verapamil, however, was not influenced by hypoxia. CSE inhibited the production of PGI2 in normoxic PAECs but did not further reduce 6-keto-PGF in hypoxic PAECs medium. The results suggested that a) the production of PGI2 during hypoxia might be stimulated by vasoactive mediators produced during hypoxia, not by hypoxia directly; b) the production and release of PGI, were related to intracellular calcium, c) the augmented production of PGI2 might be one of the mechanisms in the pulmonary vasodilating role of PAF: and d) prostaglandin production might be associated with the alteration of hypoxic pulmonary vasoreactivity after cigarette smoking.

Original languageEnglish (US)
Pages (from-to)6-9
Number of pages4
JournalJournal of Tongji Medical University
Issue number1
Publication statusPublished - Mar 1 1991
Externally publishedYes



  • hypoxia
  • prostaglandins
  • pulmonary circulation
  • smoking
  • vascular endothelium

ASJC Scopus subject areas

  • Management of Technology and Innovation

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