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静脉注射β-拟交感神经药物抑制宫缩对人胎儿血清促红细胞生成素水平的影响。

Effect of intravenous beta-sympathomimetic tocolysis on human fetal serum erythropoietin levels.

作者信息

Rouse D J, Widness J A, Weiner C P

机构信息

Department of Obstetrics and Gynecology, University of Iowa Hospitals and Clinics, Iowa City.

出版信息

Am J Obstet Gynecol. 1993 Apr;168(4):1278-82. doi: 10.1016/0002-9378(93)90380-2.

DOI:10.1016/0002-9378(93)90380-2
PMID:8475975
Abstract

OBJECTIVE

The major stimulus for erythropoietin production is tissue hypoxia. We sought to investigate the relationship of beta-sympathomimetic administration for tocolysis and fetal serum erythropoietin.

STUDY DESIGN

Umbilical cord blood was obtained from infants whose mothers received intravenous beta-sympathomimetic tocolysis and who were delivered at < or = 34 weeks' gestation. Serum erythropoietin was measured by radioimmunoassay. On the basis of the presumed 2- to 4-hour half-life of fetal erythropoietin, the infants were divided into two groups. In group 1 (n = 16) beta-sympathomimetic therapy was discontinued < 24 hours before delivery; in group 2 (n = 11) it was discontinued > or = 24 hours before delivery.

RESULTS

Group 1 fetuses had significantly higher erythropoietin levels than did group 2 fetuses (37.3 vs 13.9 mU/ml, p = 0.02). The duration of beta-sympathomimetic tocolysis and the maximum infusion rate were not different. The two groups did not differ in gestational age, birth weight, route of delivery, presence of labor, or duration of first or second stage of labor.

CONCLUSIONS

We speculate that intravenous beta-sympathomimetic tocolytic therapy stimulates fetal erythropoietin production by decreasing fetal oxygenation as a result of the reversible fetal metabolic effects of the tocolysis. These data suggest that beta-sympathomimetic tocolysis should be undertaken cautiously if fetal compromise is suspected, fetal well-being should be assessed carefully if tocolysis is undertaken, and treatment should be discontinued promptly if a clear benefit is not realized.

摘要

目的

促红细胞生成素产生的主要刺激因素是组织缺氧。我们试图研究使用β-拟交感神经药进行安胎治疗与胎儿血清促红细胞生成素之间的关系。

研究设计

从母亲接受静脉注射β-拟交感神经药安胎治疗且在妊娠≤34周时分娩的婴儿中获取脐带血。通过放射免疫测定法测量血清促红细胞生成素。根据胎儿促红细胞生成素假定的2至4小时半衰期,将婴儿分为两组。第1组(n = 16)在分娩前<24小时停止β-拟交感神经药治疗;第2组(n = 11)在分娩前≥24小时停止治疗。

结果

第1组胎儿的促红细胞生成素水平显著高于第2组胎儿(37.3对13.9 mU/ml,p = 0.02)。β-拟交感神经药安胎治疗的持续时间和最大输注速率并无差异。两组在胎龄、出生体重、分娩方式、是否临产或第一产程或第二产程的持续时间方面并无差异。

结论

我们推测静脉注射β-拟交感神经药安胎治疗通过因安胎治疗的可逆性胎儿代谢效应降低胎儿氧合作用,从而刺激胎儿促红细胞生成素的产生。这些数据表明,如果怀疑有胎儿窘迫,应谨慎进行β-拟交感神经药安胎治疗;如果进行安胎治疗,应仔细评估胎儿状况;如果未明显获益,应立即停止治疗。

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