Katz V L, Seeds J W
Department of Obstetrics and Gynecology, University of North Carolina School of Medicine, Chapel Hill 27514.
Am J Obstet Gynecol. 1989 Jul;161(1):1-4. doi: 10.1016/0002-9378(89)90219-6.
beta-Sympathomimetic drugs cross the placenta freely. Just as these agents cause serious cardiovascular changes in the mother, they may cause severe cardiovascular complications in the fetus. beta-Sympathomimetic agents for tocolysis have been associated with fetal heart rate and rhythm disturbances, hydrops, stillbirth, neonatal cardiac failure, myocardial ischemia and infarction, and neonatal death. Prospective studies have documented changes in interventricular septa of babies exposed to these drugs. Histologic changes have been reproduced in animal models and in vitro similar to those seen in infants with myocardial disease caused by beta-mimetic therapy. The mechanism of beta-mimetic toxicity appears to be increased myocardial intracellular calcium leading to overexcitation and cell necrosis. Since serious fetal cardiovascular effects may occur with beta-mimetic use, benefits should clearly outweigh risks before these drugs are administered.
β-拟交感神经药物可自由通过胎盘。正如这些药物会在母亲体内引起严重的心血管变化一样，它们也可能在胎儿体内导致严重的心血管并发症。用于抑制宫缩的β-拟交感神经药物与胎儿心率和节律紊乱、水肿、死产、新生儿心力衰竭、心肌缺血和梗死以及新生儿死亡有关。前瞻性研究记录了接触这些药物的婴儿室间隔的变化。在动物模型和体外实验中已再现了与β-拟交感神经治疗引起的心肌疾病婴儿相似的组织学变化。β-拟交感神经毒性的机制似乎是心肌细胞内钙增加，导致过度兴奋和细胞坏死。由于使用β-拟交感神经药物可能会对胎儿心血管产生严重影响，因此在使用这些药物之前，其益处应明显大于风险。
