Männistö J, Uotila P
Prostaglandins. 1982 Jun;23(6):833-9. doi: 10.1016/0090-6980(82)90127-7.
The effects of cigarette smoke on the metabolism of exogenous PGE2 and PGF2 alpha were investigated in isolated rat and hamster lungs. When isolated lungs from animals were ventilated with cigarette smoke during pulmonary infusion of 100 nmol of PGE2 or PGF2 alpha, the amounts of the 15-keto-metabolites in the perfusion effluent were decreased. Pre-exposure of animals to cigarette smoke daily for 3 weeks did not change the metabolism of PGE2 when the lungs were ventilated with air. Cigarette smoke ventilation of lungs from pre-exposed animals caused, however, a similar decrease in the metabolism of PGE2 as in animals not previously exposed to smoke. After pulmonary injection of 10 nmol of 14C-PGE2 the radioactivity appeared more rapidly in the effluent during cigarette smoke ventilation suggesting inhibition of the PGE2 uptake mechanism. In rat lungs pulmonary vascular pressor responses to PGE2 and PGF2 alpha were inhibited by smoke ventilation.
在离体大鼠和仓鼠肺中研究了香烟烟雾对外源性前列腺素E2(PGE2)和前列腺素F2α(PGF2α)代谢的影响。当在肺灌注100纳摩尔PGE2或PGF2α期间用香烟烟雾对动物的离体肺进行通气时,灌注流出液中15-酮代谢物的量减少。每天让动物预先暴露于香烟烟雾中3周,当肺用空气通气时,PGE2的代谢没有改变。然而,对预先暴露动物的肺进行香烟烟雾通气,导致PGE2代谢的降低与未预先暴露于烟雾的动物相似。在肺注射10纳摩尔14C-PGE2后,在香烟烟雾通气期间流出液中的放射性出现得更快,表明PGE2摄取机制受到抑制。在大鼠肺中,香烟烟雾通气抑制了对PGE2和PGF2α的肺血管升压反应。