Bourbon J R, Hoffman D R, Johnston J M
Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas 75235.
Exp Lung Res. 1991 Jul-Aug;17(4):789-801. doi: 10.3109/01902149109062878.
Platelet-activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine, or PAF) has previously been shown to induce glycogenolysis in the perfused adult rat liver and in the lung and liver of 24 day (gestational age) fetal rabbits in utero. In the present report, the effect of PAF was examined in fetal rats that were intravenously injected (through the vitellin vein) at a stage in their gestational development characterized by rapid glycogen depletion and surfactant accumulation. At 24 h after PAF administration of 2.5 micrograms and 5.0 micrograms to 19.5- and 20.5-day-old fetal rats, respectively, the lung glycogen content decreased significantly. In contrast, the inactive enantiomer of PAF did not modify the glycogenolytic response in vivo. When [14C]glucose (5 muCi) and PAF (5 micrograms) were simultaneously injected through the vitellin vein of the fetus, the radioactivity incorporated into lung glycogen was reduced as compared with control fetuses receiving the vehicle alone. An additional effect of PAF was noted in experiments designed to correlate glycogen breakdown to surfactant phospholipid biosynthesis. An inhibition of [3H]choline uptake and incorporation into phospholipids of fetal human lung explants and fetal lung type II pneumonocytes was induced by PAF. It is concluded that PAF appears to be a potential inducer of glycogen breakdown in the fetal lung and the relationship of these findings to fetal lung maturation is discussed.
血小板活化因子（1-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱，即PAF）先前已被证明可在灌注的成年大鼠肝脏以及子宫内24日龄（胎龄）胎兔的肺和肝脏中诱导糖原分解。在本报告中，研究了PAF对处于胎龄发育阶段、以糖原快速消耗和表面活性剂积聚为特征的胎鼠的影响。分别向19.5日龄和20.5日龄的胎鼠静脉注射（通过卵黄静脉）2.5微克和5.0微克的PAF，在给药24小时后，肺糖原含量显著降低。相比之下，PAF的无活性对映体在体内并未改变糖原分解反应。当通过胎儿的卵黄静脉同时注射[14C]葡萄糖（5微居里）和PAF（5微克）时，与仅接受赋形剂的对照胎儿相比，肺糖原中掺入的放射性降低。在旨在将糖原分解与表面活性剂磷脂生物合成相关联的实验中还发现了PAF的另一个作用。PAF可诱导抑制胎儿人肺外植体和胎儿肺II型肺细胞对[3H]胆碱的摄取及其掺入磷脂的过程。得出的结论是，PAF似乎是胎儿肺中糖原分解的潜在诱导剂，并讨论了这些发现与胎儿肺成熟的关系。
