Understanding preterm labor
Understanding preterm labor
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DOI：
10.1111/j.1749-6632.2001.tb03804.x
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发表时间：
2001-01-01
期刊：
影响因子：
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通讯作者：
Alfaidy, N
中科院分区：
文献类型：
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作者：
Challis, JRG;Lye, SJ;Alfaidy, N
足月和早产时子宫收缩力的增加是由于子宫肌层的激活和刺激所致。子宫的机械拉伸和胎儿下丘脑-垂体-肾上腺 (HPA) 轴活动增加导致的内分泌途径可以激发激活。在胎羊中，怀孕期间皮质醇输出增加以雌激素独立的方式调节胎盘中前列腺素 H 合酶 2 (PGHS2) 的表达，导致胎儿循环中 PGE(2) 水平增加。随后，母体子宫 PGHS2 表达的增加需要雌激素升高，并导致母体循环中 PGF(2)α 浓度增加。因此，足月时 PGHS2 的调节在胎儿（滋养层）和母体（子宫上皮）组织中受到不同的控制。这种差异可能反映了胎盘滋养层细胞中糖皮质激素受体（GR）的表达，而不是雌激素受体（ER）的表达。在女性中，皮质醇还通过上调 PGHS2（羊膜和绒毛膜）和下调 15-OH PG 脱氢酶（绒毛膜滋养层）来增加胎儿组织中 PG 的产生。皮质醇对绒毛膜 PGDH 表达的影响可能通过旁分泌或自分泌作用逆转黄体酮的强直刺激作用。我们将这种相互作用解释为灵长类动物中与出生相关的“黄体酮撤退”的反映。其他药物，例如促炎细胞因子，类似地上调 PGHS2 并降低 PGDH 的表达，表明存在多种可能启动足月或早产的机制。在制定早产患者的检测和管理策略时需要考虑这些不同的机制。
Increased uterine contractility at term and preterm results from activation and then stimulation of the myometrium. Activation can be provoked by mechanical stretch of the uterus and by an endocrine pathway resulting from increased activity of the fetal hypothalamic-pituitary-adrenal (HPA) axis. In fetal sheep, increased cortisol output during pregnancy regulates prostaglandin H synthase type 2 (PGHS2) expression in the placenta in an estrogen-independent manner, resulting in increased levels of PGE(2) in the fetal circulation. Later increases in maternal uterine expresssion of PGHS2 require elevations of estrogen and lead to increased concentrations of PGF(2)alpha in the maternal circulation. Thus, regulation of PGHS2 at term is differentially controlled in fetal (trophoblast) and maternal (uterine epithelium) tissue. This difference may reflect expression of the glucocorticoid receptor (GR), but not estrogen receptor (ER), in placental trophoblast cells. In women, cortisol also contributes to increased PG production in fetal tissues through upregulation of PGHS2 (amnion and chorion) and downregulation of 15-OH PG dehydrogenase (chorion trophoblasts). The effect of cortisol on chorion expression of PGDH reverses a tonic stimulatory effect of progesterone, potentially through a paracrine or autocrine action. We have interpreted this interaction as a reflection of "progesterone withdrawal" in the primate, in relation to birth. Other agents, such as proinflammatory cytokines, similarly upregulate PGHS2 and decrease expression of PGDH, indicating the presence of several mechanisms by which labor at term or preterm may be initiated. These different mechanisms need to be considered in the development of strategies for the detection and management of the patient in preterm labor.