Domer F R, Boertje S B, Sampson J B
Res Commun Chem Pathol Pharmacol. 1985 Apr;48(1):27-37.
Charles River, Sprague-Dawley rats of both sexes were anesthetized with pentobarbital sodium, 50 mg/kg i.p. and a jugular vein and femoral artery cannulated. Saline, arachidonic acid (1, 2, 4 or 6 mg/kg) alone or 15 minutes after administration of indomethacin (5 mg/kg), prostaglandin E2 (0.5, 1, 2 or 4 micrograms/kg) (PGE2), prostaglandin F2 alpha (20, 40, 80 or 160 micrograms/kg) (PGF2 alpha) or prostaglandin I2 (prostacyclin) (0.5, 1, 2 or 4 micrograms/kg) (PGI2) were given intravenously. Each of the drugs caused a dose-dependent decrease in blood pressure except for PGF2 alpha which caused an initial, short-lasting fall in blood pressure followed by a more sustained rise in blood pressure. The permeability of the blood-brain barrier was measured using 99mTc-sodium pertechnetate (TcO-4). None of the prostaglandins or arachidonic acid caused a significant change in the permeability of the blood-brain barrier. This provides a further example of a dissociation between drug-induced changes in systemic blood pressure and change in the permeability of the blood-brain barrier.
采用50mg/kg腹腔注射戊巴比妥钠对雄性和雌性的查尔斯河斯普拉格-道利大鼠进行麻醉，并对其颈静脉和股动脉进行插管。单独静脉注射生理盐水、花生四烯酸（1、2、4或6mg/kg），或在注射吲哚美辛（5mg/kg）15分钟后，静脉注射前列腺素E2（0.5、1、2或4μg/kg）（PGE2）、前列腺素F2α（20、40、80或160μg/kg）（PGF2α）或前列腺素I2（前列环素）（0.5、1、2或4μg/kg）（PGI2）。除PGF2α外，每种药物均导致血压呈剂量依赖性下降，PGF2α最初导致血压短暂下降，随后血压持续升高。使用高锝酸钠（TcO-4）测量血脑屏障的通透性。前列腺素或花生四烯酸均未引起血脑屏障通透性的显著变化。这进一步证明了药物引起的全身血压变化与血脑屏障通透性变化之间的分离。
