Maas D L, Martinson D R, Erdmann M D, Wahle J S, Hagen T C
Department of Medicine, Medical College of Wisconsin, Milwaukee 53226, USA.
Proc Soc Exp Biol Med. 1995 Nov;210(2):150-5. doi: 10.3181/00379727-210-43934.
Experiments were performed to determine whether PRL secretion in the rat diethylstilbestrol (DES)-induced prolactinoma model is affected by the addition of thyrotropin-releasing hormone (TRH) and/or immunoneutralization of intrapituitary vasoactive intestinal polypeptide (VIP) in vitro. Male Fischer 344 rats were implanted with either a 10 mg DES or placebo pellet 30 days prior to obtaining the anterior pituitary glands for perifusion. The anterior pituitaries were quartered and used in three different perifusion experiments. In Experiment I, placebo-treated tissue channels were perifused for 2 baseline hr followed consecutively by a 30-min exposure to 1:100 nonimmune rabbit serum (NRS), a 30-min wash, and a final 30-min exposure to 10(-5) M TRH. Additional placebo channels were run as above except 1:100 VIP antiserum (AVIP) was substituted for NRS and AVIP was added to the TRH. In Experiment II, the same perifusion protocol was used as in Experiment I, except DES-induced tumor tissue was used instead of placebo tissue. Results from Experiment I and II reveal that AVIP significantly decreased PRL secretory rate in both DES and placebo groups. In the tumor group, both TRH alone and in the presence of AVIP significantly increased the PRL secretory rate. In Experiment III DES-induced tumor tissue channels were perifused with a similar protocol, except the concentrations of NRS and AVIP were increased to 1:10. Both NRS and AVIP significantly decreased PRL secretory rate; however, AVIP had a significantly greater effect than NRS. In this experiment, 1:10 AVIP overcame the stimulatory effect of TRH. In conclusion, AVIP decreases and TRH increases, even in the presence of AVIP, PRL release in DES-induced prolactinoma tissue in vitro. Increasing the AVIP concentration 10-fold diminished the PRL-releasing action of TRH in the tumor tissue. These data suggested that PRL secretion is not autonomous in these prolactinomas and can be affected by exogenous TRH and partial immunoneutralization of endogenous VIP.
进行实验以确定在大鼠己烯雌酚（DES）诱导的催乳素瘤模型中，催乳素（PRL）分泌是否受体外添加促甲状腺激素释放激素（TRH）和/或垂体血管活性肠肽（VIP）免疫中和的影响。在获取用于灌流的垂体前叶前30天，给雄性Fischer 344大鼠植入10 mg DES或安慰剂药丸。将垂体前叶切成四等份，用于三个不同的灌流实验。在实验I中，对安慰剂处理的组织通道进行2小时基线灌流，随后依次进行30分钟1:100非免疫兔血清（NRS）暴露、30分钟冲洗以及最后30分钟10⁻⁵ M TRH暴露。除用1:100 VIP抗血清（AVIP）替代NRS并在TRH中加入AVIP外，额外的安慰剂通道按上述方法进行。在实验II中，使用与实验I相同的灌流方案，但用DES诱导的肿瘤组织替代安慰剂组织。实验I和II的结果表明，AVIP显著降低了DES组和安慰剂组的PRL分泌率。在肿瘤组中，单独使用TRH以及在有AVIP存在时均显著提高了PRL分泌率。在实验III中，对DES诱导的肿瘤组织通道采用类似方案进行灌流，但将NRS和AVIP的浓度提高到1:10。NRS和AVIP均显著降低了PRL分泌率；然而，AVIP的作用明显大于NRS。在该实验中，1:10 AVIP克服了TRH的刺激作用。总之，AVIP降低而TRH增加（即使存在AVIP）体外DES诱导的催乳素瘤组织中的PRL释放。将AVIP浓度提高10倍可减弱TRH在肿瘤组织中的PRL释放作用。这些数据表明，这些催乳素瘤中的PRL分泌并非自主的，且可受外源性TRH和内源性VIP部分免疫中和的影响。
