INTERLEUKIN 1 INFUSION DECREASES DECIDUAL PROLACTIN SECRETION IN PRIMATES

灵长类动物的羊水中含有高浓度的 蜕膜来源的催乳素(PRL)，随着宫内的减少 早产前的细菌感染。细胞因子和 羊水前列腺素(PGs)感染后升高 体内和细胞因子在体外抑制蜕膜PRL的分泌。至 确定细胞因子或前列腺素是否介导细菌的作用 对整个动物PRL的感染，慢性仪器化 准备好怀孕的恒河猴。白介素1(10 FG；6 M l/h，2 h)单独注入羊膜腔(n=6)， 在长期使用消炎痛治疗期间(n=5)。在动物身上 连续接受两种治疗(n=4)，静脉滴注 吲哚美辛先于IL-1单独输注，因为IL-1可以 诱导早产。取羊水标本进行相关分析 在-24小时和-1小时输液，然后在以下期间至少输液一次 24小时，然后在25小时到72小时之间。样品在-20℃下冷冻 直到PRL化验。羊水中IL-1水平得到证实， 同时测定前列腺素E_2和前列腺素F_2。PRL水平表示为 预输注值百分比，经方差分析比较 然后是两两比较。IL-1水平大于10 ng/ml 都是由于输液而实现的。吲哚美辛期间PG不变 治疗，但在单独使用IL-1后显著增加。在.之前 IL-1输注后，PRL水平平均为82q 20fg/ml。 导致羊水催乳素在24小时内下降42%(p&lt；0.05 vs 预先输注)，72小时下降66%(P&lt；0.05比24小时)。当时有一场 输液后2.4h子宫活动度增加6.0q。其中五项 6只动物在输注IL-1 29h后74q出生。 在IL-1之前输注吲哚美辛48小时，然后输注60小时 IL-1不能阻断IL-1对PRL水平下降的影响。 PRL水平在输液后25-72小时比输液前低41% 在消炎痛存在的情况下输注(p&lt；0.05)。吲哚美辛干的 预防IL-1诱导的子宫活动增加 独自一人。综上所述，IL-1导致羊水催乳素水平下降。 类似于细菌感染的方式。封锁PG生产 阻止了子宫收缩，但并没有阻止子宫收缩的下降 羊水PRL。这些结果支持了IL-1可能 直接作用于蜕膜细胞，抑制催乳素分泌。

Amniotic fluid of primates contains a high concentration of prolactin (PRL) of decidual origin which decreases with intrauterine bacterial infection prior to preterm labor. Cytokines and prostaglandins (PGs) increase in amniotic fluid after infection in vivo and cytokines inhibit decidual PRL secretion in vitro. To determine whether cytokines or PGs mediate the effect of bacterial infection on PRL in the whole animal, chronically instrumented pregnant rhesus monkeys were prepared. Interleukin (IL)-1 (10 fg; 6 ml/h for 2 h) was infused into the amniotic cavity, alone (n=6) and during a longer term treatment with indomethacin (n=5). In animals which received both treatments serially (n=4), the infusion with indomethacin preceded the infusion of IL-1 alone because IL-1 can induce preterm labor. Amniotic fluid samples were obtained relative to infusion at -24 h and -1 h, then at least once during the following 24 h, and again between 25 h and 72 h. Samples were frozen at -20xC until assay for PRL. Amniotic fluid levels of IL-1 were verified and PGE2 and PGF2` were also measured. PRL levels were expressed as a percent of preinfusion values and compared by analysis of variance followed by pairwise comparison. IL-1 levels greater than 10 ng/ml were achieved due to infusion. PGs were unchanged during indomethacin treatment, but increased significantly following IL-1 alone. Prior to IL-1 infusion, PRL levels averaged 82 q 20 fg/ml. Infusion of IL-1 caused a 42% decrease in amniotic fluid PRL by 24 h (p<0.05 vs preinfusion) and a 66% decline by 72 h (p<0.05 vs 24 h). There was an increase in uterine activity at 6.0 q 2.4 h after infusion. Five of the 6 animals delivered at 74 q 29 h after infusion of IL-1 . Infusion of indomethacin for 48 h preceding IL-1 plus 60 h following IL-1 did not abolish the effect of IL-1 on the decline in PRL levels. PRL levels were 41% less than preinfusion values by 25-72 h post infusion (p<0.05) in the presence of indomethacin. Indomethacin did prevent the increase in uterine activity which was induced by IL-1 alone. In summary, IL-1 caused a decrease in amniotic fluid PRL in a manner similar to bacterial infection. Blockade of PG production prevented uterine contractions but it did not prevent the decline in amniotic fluid PRL. These results support the notion that IL-1 may act directly on decidual cells and inhibit PRL secretion.