Husslein P
Z Geburtshilfe Perinatol. 1985 May-Jun;189(3):95-102.
Questions related to the mechanism of human labor are of central clinical importance nowadays, since the majority of perinatal mortality and morbidity is due to disregulation of uterine contractility mainly premature onset of labor. During delivery of spontaneous or induced onset endogenous prostaglandin F-synthesis increases dramatically and reaches a maximum at the time of placental separation. These increased amounts of prostaglandin F and E lead to myometrial contractions and to a reduction of the cervical resistance. Post partum, prostaglandins lead to the contracture of the myometrium necessary for separation and expulsion of the placenta. The precise causes for initiation of parturition at term however have not been fully elucidated. The present review presents a theory in which oxytocin acts as central trigger of labor. At the end of human pregnancy a marked rise in the concentration of oxytocin receptors in the myometrium can be observed, thereby leading to an increased sensitivity of the myometrium towards oxytocin. Therefore, a small increase of the circulating oxytocin concentration in the maternal peripheral blood (for example through addition of fetal oxytocin) is sufficient to induce contractions. Apart from inducing contractions, oxytocin also leads to a stimulation of prostaglandin synthesis through receptors in the decidua. Prostaglandins themselves lead to further contractions, soften the cervix, induce gap-junctions and sensitize the myometrium further for oxytocin, thereby leading to a progressive cervical dilatation. At the end of the first stage of labor, the membranes usually rupture leading to a further increase in prostaglandin synthesis, so that the mechanism can no longer be interrupted exogenously.(ABSTRACT TRUNCATED AT 250 WORDS)
如今,与人类分娩机制相关的问题具有至关重要的临床意义,因为围产期的大多数死亡和发病是由于子宫收缩失调,主要是早产。在自然分娩或引产过程中,内源性前列腺素F的合成会急剧增加,并在胎盘分离时达到峰值。这些增加的前列腺素F和E会导致子宫肌层收缩,并降低宫颈阻力。产后,前列腺素会导致子宫肌层收缩,这对于胎盘的分离和排出是必要的。然而,足月分娩开始的确切原因尚未完全阐明。本综述提出了一种理论,即催产素是分娩的核心触发因素。在人类妊娠末期,可以观察到子宫肌层中催产素受体浓度显著升高,从而导致子宫肌层对催产素的敏感性增加。因此,母体外周血中循环催产素浓度的小幅增加(例如通过添加胎儿催产素)就足以诱发宫缩。除了诱发宫缩外,催产素还会通过蜕膜中的受体刺激前列腺素的合成。前列腺素本身会导致进一步的宫缩,软化宫颈,诱导缝隙连接,并使子宫肌层对催产素更加敏感,从而导致宫颈逐渐扩张。在第一产程结束时,胎膜通常会破裂,导致前列腺素合成进一步增加,因此这种机制无法再通过外源方式被打断。(摘要截选至250字)