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. 2016 Jun 28;4(12):e12840. doi: 10.14814/phy2.12840

Figure 2.

Figure 2

A, Baseline production of prostacyclin and thromboxane by fetal and newborn pulmonary artery smooth muscle cells (PASMC). Release of prostacyclin (PGI2) and thromboxane (TxA2) by fetal and newborn PASMC at baseline was measured by ELISA of their respective stable metabolites 6‐keto‐PGF1α and TxB2. Data are mean + SEM, n = 6. Production of 6‐keto‐PGF1α by newborn PASMC was ninefold greater than by fetal PASMC, whereas baseline production of TxB2 by newborn PA was sevenfold less. *P < 0.05, different from fetal PA. B, Hyperoxia attenuates prostacyclin release by newborn PASMC. Effect of hypoxia and hyperoxia on prostacyclin release was measured as 6‐keto‐PGF1α. Data are mean ± SEM, n = 6. Hyperoxia attenuated prostacyclin release under all conditions. Inhibition of PAFR with CV3988 increased prostacyclin release. *P < 0.05, different from normoxia; + P < 0.05, different from hypoxia and hyperoxia; **P < 0.05, different from CV3988 or flurbiprofen normoxia; # P < 0.05, different Baseline and CV3988 conditions.