Kobayashi T, Morita I, Murota S
Prostaglandins. 1983 Aug;26(2):303-10. doi: 10.1016/0090-6980(83)90097-7.
Effects of nitrogen dioxide (NO2) exposure on prostacyclin (PGI2) synthesis in the rat lung and thromboxane A2 (TXA2) synthesis in the platelets were studied. Male Wistar rats were exposed to 10 ppm NO2 for 1, 3, 5, 7 and 14 days. PGI2 synthesizing activity of homogenized lung decreased. The damage of PGI2 synthesizing activity reaches its maximum at 3 days. At 14 days, PGI2 synthesizing activity returned to the normal level. The activity of PGI2 synthetase decreased significantly. The formation of lipid peroxides due to NO2 exposure may cause the depression of PGI2 synthesizing activity of lung. On the other hand, platelet TXA2 synthesizing activity increased. This increased TXA2 synthesizing activity lasted at least till 3 days. Then, it returned to the normal level. The counts of platelet were decreased significantly by 1, 3, 5 and 7 days NO2 exposure. Then the decreased counts of platelet returned to the normal level at 14 days NO2 exposure. These results indicate that the depression of PGI2 synthesizing activity of lung by NO2 exposure cause an increase in TXA2 synthesizing activity of platelets. It may contribute to induce platelet aggregation and to the observed decrease in the number of platelets during NO2 exposure.
研究了二氧化氮(NO₂)暴露对大鼠肺中前列环素(PGI₂)合成及血小板中血栓素A₂(TXA₂)合成的影响。将雄性Wistar大鼠暴露于10 ppm的NO₂中1、3、5、7和14天。肺匀浆的PGI₂合成活性降低。PGI₂合成活性的损伤在3天时达到最大值。在14天时,PGI₂合成活性恢复到正常水平。PGI₂合成酶的活性显著降低。NO₂暴露导致的脂质过氧化物形成可能会引起肺PGI₂合成活性的降低。另一方面,血小板TXA₂合成活性增加。这种增加的TXA₂合成活性至少持续到3天。然后,它恢复到正常水平。暴露于NO₂ 1、3、5和7天会使血小板计数显著降低。然后,在暴露于NO₂ 14天时,降低的血小板计数恢复到正常水平。这些结果表明,NO₂暴露导致的肺PGI₂合成活性降低会引起血小板TXA₂合成活性增加。这可能有助于诱导血小板聚集以及在NO₂暴露期间观察到的血小板数量减少。