Camussi G, Montrucchio G, Antro C, Bussolino F, Tetta C, Emanuelli G
Immunopharmacology. 1983 Aug;6(2):87-96. doi: 10.1016/0162-3109(83)90002-4.
Synthetic platelet-activating factor (PAF) (1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine, AGEPC) has been shown to induce a slowly developing contraction of rabbit lung parenchymal strips in an isolated organ bath. The spasmogenic effect of AGEPC appeared to be mediated by specific receptors distinct from H1, H2, cholinergic and C5a anaphylatoxin receptors. Prior exposure to AGEPC induced specific desensitization of lung parenchymal strips. Experiments with several pharmacological agents indicated that AGEPC-induced contraction was independent from cyclooxygenase, but was blocked when phospholipase A2 and lipoxygenase were inhibited and when the Ca++ channels were antagonized. Corticosteroids exhibited an inhibitory effect specific for AGEPC. Intracellular levels of cyclic AMP or cyclic GMP seemed to have a modulatory role in AGEPC-induced contraction of rabbit lung parenchymal strips.
合成血小板激活因子（PAF）（1-0-十八烷基-2-乙酰基-sn-甘油-3-磷酸胆碱，AGEPC）已被证明在离体器官浴中可诱导兔肺实质条带缓慢发展的收缩。AGEPC的致痉挛作用似乎由不同于H1、H2、胆碱能和C5a过敏毒素受体的特异性受体介导。预先暴露于AGEPC可诱导肺实质条带的特异性脱敏。使用几种药理剂的实验表明，AGEPC诱导的收缩与环氧化酶无关，但当磷脂酶A2和脂氧合酶被抑制以及钙离子通道被拮抗时，收缩被阻断。皮质类固醇对AGEPC表现出特异性抑制作用。环磷酸腺苷（cAMP）或环磷酸鸟苷（cGMP）的细胞内水平似乎在AGEPC诱导的兔肺实质条带收缩中具有调节作用。
