Myers R E
Pavlov J Biol Sci. 1977 Jan-Mar;12(1):51-62. doi: 10.1007/BF03001799.
Several lines of evidence indicate that maternal psychological stress leads to adverse pregnancy outcome in rhesus monkey. Chronic anxiety causes an increased stillbirth rate, fetal growth retardation, and altered placental morphology. On another time scale, lightening of maternal anesthesia during surgery produces an impaired fetal oxygenation while re-institution of anesthesia ameliorates the fetal asphyxia. The present study, for the first time, demonstrates a relationship between specific episodes of meternal psychological stress and exacerbation of fetal asphyxia in utero. Eight term pregnant rhesus monkeys were anesthetized with sodium pentobarbital. Catheters were placed both into the maternal and the fetal femoral arteries for the continuous recording of blood pressure and heart rate and for the intermittent campling of maternal and fetal blood. An open-ended catheter recorded intrauterine pressures. Following a complete repair, the anesthesia of the mothers was allowed to lighten. As the mothers awakened, the fetuses invariably showed the developemnt of fetal asphyxia. A fetal acidosis developed and the fetal oxygenation and repair of acidosis. Studies while the mothers were fully awake showed the repeated and regular development of episodes of heightened fetal asphyxia produced by episodes of stressful stimulation of the mothers. Episodes of maternal psychological stress led to changes in both fetal vital signs and blood chemical findings. These alterations in fetal state regularly followed the onset of the episodes of psychological stress by 50 seconds. These changes also usually remitted 50 seconds following the termination of the periods of stress. These results demonstrated a direct and unequivocal relationship between meternal psychological stress and fetal asphyxia. It is assumed the maternal stress produces impairments in the circulation to the uterus through an increased sympathetic nervous system activity and a shunting of the maternal blood-flow from the abdominal viscera to other organs as occurs in the fight-orflight reaction.
多项证据表明,母体心理压力会导致恒河猴出现不良妊娠结局。慢性焦虑会导致死产率增加、胎儿生长受限以及胎盘形态改变。在另一个时间尺度上,手术期间母体麻醉减轻会导致胎儿氧合受损,而重新麻醉则可改善胎儿窒息状况。本研究首次证明了母体心理压力的特定发作与子宫内胎儿窒息加重之间的关系。八只足月妊娠的恒河猴用戊巴比妥钠麻醉。将导管分别插入母体和胎儿的股动脉,以连续记录血压和心率,并间歇性采集母体和胎儿血液样本。一根开放式导管记录子宫内压力。在完全修复后,允许母体麻醉减轻。随着母体苏醒,胎儿 invariably 出现胎儿窒息的发展。出现胎儿酸中毒以及胎儿氧合和酸中毒的修复。在母体完全清醒时进行的研究表明,母体受到应激刺激时,胎儿窒息发作会反复且有规律地出现。母体心理压力发作会导致胎儿生命体征和血液化学指标发生变化。胎儿状态的这些改变通常在心理压力发作开始后 50 秒出现。这些变化通常也会在压力期结束后 50 秒缓解。这些结果证明了母体心理压力与胎儿窒息之间存在直接且明确的关系。据推测,母体压力通过增加交感神经系统活动以及使母体血液从腹腔内脏分流到其他器官,就像在战斗或逃跑反应中发生的那样,从而对子宫循环产生损害。