Mais D E, Bosin T R
Toxicol Lett. 1984 Aug;22(2):255-9. doi: 10.1016/0378-4274(84)90075-4.
Exposure of mice to normobaric 100% oxygen for 24-96 h is known to damage the pulmonary capillary endothelium and alter the disposition of serotonin (5-hydroxytryptamine, 5-HT). We now report that such exposure increased the concentration of platelets and decreased the platelet content of 5-HT and a tracer dose of [3H]5-HT. After 48 h of hyperoxia exposure, the platelet concentration was elevated to 121% of air-exposed control values and the content of 5-HT and [3H]5-HT/10(9) platelets was decreased 76% and 57%, respectively. Kinetic analysis of the platelet 5-HT uptake process indicated that hyperoxia exposure caused an increased affinity and decreased velocity of transport. After 48 h of oxygen exposure the Km for platelet 5-HT uptake was 1.91 +/- 0.67 X 10(-7) M and the Vmax 30.1 +/- 4.6 pmol/10(8) platelets/4 min compared to air-exposed control values of Km 3.37 +/- 0.32 X 10(-7) M and Vmax 46.7 +/- 3.5 pmol/10(8) platelets/4 min, respectively. These changes in platelet 5-HT uptake and disposition may contribute to the pathophysiology of the pulmonary microvascular response to hyperoxia-induced injury.
已知将小鼠暴露于常压100%氧气环境中24 - 96小时会损伤肺毛细血管内皮，并改变血清素（5 - 羟色胺，5 - HT）的分布。我们现在报告，这种暴露会增加血小板浓度，并降低血小板中5 - HT的含量以及示踪剂量的[3H]5 - HT的含量。在高氧暴露48小时后，血小板浓度升高至空气暴露对照组值的121%，而5 - HT和[3H]5 - HT/10(9)血小板的含量分别降低了76%和57%。血小板5 - HT摄取过程的动力学分析表明，高氧暴露导致转运亲和力增加而速度降低。与空气暴露对照组相比，氧气暴露48小时后血小板摄取5 - HT的Km为1.91 +/- 0.67 X 10(-7) M，Vmax为30.1 +/- 4.6 pmol/10(8)血小板/4分钟，而空气暴露对照组的Km为3.37 +/- 0.32 X 10(-7) M，Vmax为46.7 +/- 3.5 pmol/10(8)血小板/4分钟。血小板5 - HT摄取和分布的这些变化可能有助于肺微血管对高氧诱导损伤反应的病理生理学过程。
