Toivonen H, Hartiala J, Bakhle Y S
Acta Physiol Scand. 1981 Feb;111(2):185-92. doi: 10.1111/j.1748-1716.1981.tb06723.x.
The effect of exposure of rats to high concentrations of oxygen (90-95%, normobaric) on the activation of angiotensin I to angiotensin II and on the inactivation of bradykinin, prostaglandin E2 (PGE2) and 5-hydroxytryptamine (serotonin) in the pulmonary circulation of isolated perfused rat lungs was investigated. After 36 h exposure, PGE2 survival in the pulmonary circulation increased and reached 3 times the control value after 48 h exposure. A decrease in the conversion of angiotensin I to angiotensin II was seen after 48 h exposure. No decrease in the inactivation of 5-hydroxytryptamine was seen until after 60 h exposure. At this time bradykinin inactivation was also decreased. The decrease in metabolism of angiotensin I and PGE2 following 48 h exposure to oxygen was reversed by a subsequent exposure to room air for 12 h. In these experiments, therefore, the earliest sign of oxygen toxicity was a decrease in PGE2 metabolism, a reaction associated with cells other than endothelial cells.
研究了将大鼠暴露于高浓度氧气(90 - 95%,常压)对离体灌注大鼠肺循环中血管紧张素I转化为血管紧张素II以及缓激肽、前列腺素E2(PGE2)和5 - 羟色胺(血清素)失活的影响。暴露36小时后,肺循环中PGE2的存留量增加,暴露48小时后达到对照值的3倍。暴露48小时后可见血管紧张素I向血管紧张素II的转化减少。直到暴露60小时后,5 - 羟色胺的失活才出现减少。此时缓激肽失活也减少。暴露于氧气48小时后血管紧张素I和PGE2代谢的减少在随后暴露于室内空气12小时后得以逆转。因此,在这些实验中,氧中毒的最早迹象是PGE2代谢减少,这是一种与内皮细胞以外的细胞相关的反应。