Pavlović-Kentera V, Susić D, Milenković P, Biljanović-Paunović L
Exp Hematol. 1980;8 Suppl 8:283-92.
The effect of prostaglandin synthetase inhibitors, aspirin and indomethacin, salt overload and salt depletion, as well as renomedullary dissection on serum Ep level in rats exposed to acute hypoxia was studied. Male rats were given aspirin or saline for seven days prior to the exposure to hypoxia. Other group of animals was fed salt free diet for the same period of time. Indomethacin was given on two consecutive days and renomedullary dissection was performed three weeks before exposure to hypoxia. Ep level was indirectly determined by measuring the 48 h 59Fe incorporation into RBC of mice with posthypoxic polycythemia. Hypoxia induced Ep production was diminished after blocking the PG synthesis using PG synthesis inhibitors. Salt overload, procedure known to decrease PG synthesis, had the same effect. Further on, dissection of the renal medulla, the main source of renal PG, decreased Ep production. The results indicate that PG are part of the mechanism which controls Ep production.
研究了前列腺素合成酶抑制剂、阿司匹林和吲哚美辛、盐超载和盐缺乏以及肾髓质剥离对急性缺氧大鼠血清Ep水平的影响。雄性大鼠在缺氧暴露前7天给予阿司匹林或生理盐水。另一组动物在同一时间段内喂食无盐饮食。连续两天给予吲哚美辛，并在缺氧暴露前三周进行肾髓质剥离。通过测量低氧后红细胞增多症小鼠红细胞中48小时59Fe的掺入量间接测定Ep水平。使用前列腺素合成抑制剂阻断前列腺素合成后，缺氧诱导的Ep产生减少。盐超载，一种已知会减少前列腺素合成的过程，也有同样的效果。此外，肾髓质（肾脏前列腺素的主要来源）的剥离降低了Ep的产生。结果表明，前列腺素是控制Ep产生机制的一部分。
