Robinson C, Hoult J R
Biochem Pharmacol. 1982 Mar 1;31(5):633-8. doi: 10.1016/0006-2952(82)90442-7.
Inactivation in the isolated perfused rat lung of prostaglandins (PG) D2, E1, F2 alpha, I2 and the metabolites 6-keto PGF1 alpha (=6KF1 alpha) and 13, 14-dihydro-15-keto PGF2 alpha (= KH2F2 alpha) was studied using 5 min perfusion of 7-10 ng/ml PG in Krebs' solution containing 0.02 microCi/ml tritiated PG and 4.5% bovine serum albumin (BSA). The parameters measured were (a) extent of inactivation (F2 alpha greater than E1 greater than D2 greater than 6KF1 alpha greater than I2; KH2F2 alpha unchanged), (b) the accumulation of PG within the lung measured as tissue to medium ratio (F2 alpha = D2 greater than E1 greater than 6KF1 alpha greater than I1 - KH2F2 alpha) and (c) rate of equilibration of PG within the lung measured as "wash-in t 1/2" (D2 greater than F2 alpha greater than E1 greater than I2 = 6KF1 alpha = KH2F2 alpha). Removal of sodium ions produced a small decrease in PGD2 and PGE1 breakdown but not of PGF2 alpha whereas breakdown of all PGs was markedly inhibited at 5 degrees. Removal of BSA enhanced PGE1 and PGI2 breakdown but not that of PGF2 alpha. Addition of 10% BSA inhibited PGE1 breakdown but not that of PGF2 alpha. Binding of PGs to 4.5% BSA was PGE1 = KH2F2 alpha greater than D2 greater than F2 alpha, and increased at 10% BSA or after removal of sodium ions. These data support the view that PGs must be taken up into pulmonary cells by a transmembrane carrier process as a prerequisite for enzymatic breakdown. The metabolites are then released back into the pulmonary circulation.
利用含0.02微居里/毫升氚标记前列腺素（PG）和4.5%牛血清白蛋白（BSA）的克雷布斯溶液，以7 - 10纳克/毫升PG灌注离体灌流大鼠肺5分钟，研究了前列腺素D2、E1、F2α、I2及其代谢产物6 - 酮 - PGF1α（= 6KF1α）和13,14 - 二氢 - 15 - 酮 - PGF2α（= KH2F2α）的失活情况。所测量的参数为：（a）失活程度（F2α＞E1＞D2＞6KF1α＞I2；KH2F2α无变化），（b）肺内PG的蓄积量，以组织与介质的比值衡量（F2α = D2＞E1＞6KF1α＞I1 - KH2F2α），以及（c）肺内PG的平衡速率，以“洗入t1/2”衡量（D2＞F2α＞E1＞I2 = 6KF1α = KH2F2α）。去除钠离子会使PGD2和PGE1的分解略有减少，但对PGF2α无影响，而在5℃时所有PG的分解均受到显著抑制。去除BSA会增强PGE1和PGI2的分解，但对PGF2α无影响。添加10% BSA会抑制PGE1的分解，但对PGF2α无影响。PG与4.5% BSA的结合情况为PGE1 = KH2F2α＞D2＞F2α，在10% BSA时或去除钠离子后结合增加。这些数据支持这样一种观点，即PG必须通过跨膜载体过程被肺细胞摄取，这是酶促分解的前提条件。然后代谢产物会释放回肺循环中。
