EFFECTS OF A NOVEL PROSTAGLANDIN, 8-EPI-PGF2-ALPHA, IN RABBIT LUNG INSITU
EFFECTS OF A NOVEL PROSTAGLANDIN, 8-EPI-PGF2-ALPHA, IN RABBIT LUNG INSITU
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DOI：
10.1152/ajpheart.1992.263.3.h660
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发表时间：
1992-09-01
影响因子：
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通讯作者：
NEWMAN, JH
中科院分区：
文献类型：
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作者：
BANERJEE, M;KANG, KH;NEWMAN, JH
我们确定了8-表前列腺素（PG）F2 α（花生四烯酸的非环氧合酶自由基催化产物）对肺血管张力的影响，其效力及其作用机制。将8-Epi-PGF 2 α（0.5-20 μ g）注射到10只家兔的肺动脉（PA）导管中，用含3%牛血清白蛋白的Krebs-Henseleit缓冲液原位灌注肺。使用20 μ g 8-epi-PGF 2 α时，PA压力从基线13.5 +/- 0.6增加至25.6 +/- 2.0 cmH 2 O。8-Epi-PGF 2 α导致PA压力快速升高，随后在40-60分钟内逐渐下降至基线水平。双血管闭塞显示在PA压力峰值上升时动脉阻力增加两倍。20 μ g 8-epi-PGF 2 α的PA压力升高是20 μ g环加氧酶衍生的前列腺素PGF 2 α的5倍。用150 μ M甲氨蝶呤阻断环氧合酶或用70 μ M酚妥拉明阻断α-受体都不能改变PA对8-epi-PGF 2 α的压力反应，但40 μ M SQ 29548（一种血栓烷受体拮抗剂）可以完全阻止PA对8-epi-PGF 2 α的压力反应。我们的结论是，在兔8-epi-PGF 2 α是一种有效的血管收缩剂的肺血管，这似乎是由于SQ 29548-响应血栓烷受体的激活。
We determined the effects of 8-epiprostaglandin (PG) F2alpha, a non-cyclooxygenase free radical-catalyzed product of arachidonic acid, on pulmonary vascular tone, its potency, and its mechanism of action. 8-Epi-PGF2alpha (0.5-20 mug) was injected into the pulmonary artery (PA) catheter of 10 rabbits whose lungs were perfused in situ with Krebs-Henseleit buffer solution with 3% bovine serum albumin. PA pressure increased from a baseline of 13.5 +/- 0.6 to 25.6 +/- 2.0 cmH2O with 20 mug 8-epi-PGF2alpha. 8-Epi-PGF2alpha caused a rapid rise in PA pressure followed by a gradual decline over 40-60 min to baseline levels. Double vascular occlusion revealed a twofold increase in arterial resistance at peak rise in PA pressure. The rise in PA pressure with 20 mug 8-epi-PGF2alpha was fivefold greater than with 20 mug of the cyclooxygenase-derived prostaglandin PGF2alpha. The PA pressure response to 8-epi-PGF2alpha was not altered by either cyclooxygenase blockade with 150 muM meclofenamate or a-receptor blockade with 70 muM phentolamine, but was fully prevented by 40 muM SQ 29548, a thromboxane receptor antagonist. We conclude that in rabbits 8-epi-PGF2alpha is a potent vasoconstrictor of the pulmonary vasculature, which appears to be due to the activation of SQ 29548-responsive thromboxane receptors.