부산대학교 도서관

1The aims of this study were to compare in the rat isolated perfused lung preparation, the antagonist effects of iloprost, a stable analogue of prostacyclin, and prostaglandin E1(PGE1) on the hypoxic pulmonary pressure response, and to investigate the possible involvement of KATPand KCachannels and of EDRF (NO) in these effects. In addition, iloprost and PGE1effects were compared to those of adenosine and forskolin.2Isolated lungs from male Wistar rats (260–320 g) were ventilated with 21% O2+ 5% CO2+ 74% N2(normoxia) or 5% CO2+ 95% N2(hypoxia) and perfused with a salt solution supplemented with ficoll. Glibenclamide (1 μm), charybdotoxin (0.1 μm), NG‐nitro‐L‐arginine methyl ester (l‐NAME, 100 μm) were used to block KATP, KCachannels and NO synthesis, respectively.3Iloprost, PGE1, adenosine and forskolin caused relaxation during the hypoxic pressure response. The order of potency was: iloprost > PGE1= forskolin > adenosine. EC50values were 1.91 ± 0.52 10−9M, 3.31 ± 0.58 10−7M, 3.24 ± 0.78 10−7M and 7.70 ± 1.68 10−5M, respectively. Glibenclamide, charybdotoxin and L‐NAME inhibited partially the relaxant effects of iloprost and forskolin but not those of PGE1.4It is concluded that in the rat isolated lung preparation, iloprost and forskolin but not PGE1dilate pulmonary vessels partly through KATPchannels, KCachannels and nitric oxide release. Furthermore our results suggest that the role of cyclic AMP in these effects is not unequivocal.