地塞米松或胎儿肺15-羟基前列腺素脱氢酶的作用:母体地塞米松治疗预防动脉导管未闭的可能机制

Michael Y. Tsai , David M. Brown
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引用次数: 23

摘要

据报道,产前母体糖皮质激素治疗可减少早产儿动脉导管未闭的发生率。动脉导管的通畅被认为主要是通过PGE的血管扩张作用来维持的,无论是在子宫内还是在早产儿中,肺是胎儿和新生儿中PGE的主要来源。15-羟基前列腺素脱氢酶(15-PGDH)催化将生物活性PGE转化为无活性类似物15-酮- pge2的初始反应。本研究研究了产前地塞米松治疗对妊娠20、21、22天胎鼠肺15-PGDH活性的影响。胎儿肺15-PGDH活性在妊娠20 ~ 22天增加一倍以上。0.4 mg/kg和0.8 mg/kg地塞米松处理显著提高了20日龄和21日龄胎儿的15-PGDH活性,但对22日龄胎儿无影响。我们推测,产前糖皮质激素治疗降低早产儿动脉导管未闭发生率的临床观察部分是由于糖皮质激素对胎儿和新生儿肺部以及可能其他器官中15-PGDH活性的刺激作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of dexamethasone or fetal lung 15-hydroxy-prostaglandin dehydrogenase: Possible mechanism for the prevention of patent ductus arteriosus by maternal dexamethasone therapy

Prenatal maternal glucocorticoid treatment has been reported to reduce the incidence of patent ductus arteriosus in prematurely born infants. Patency of the ductus arteriosus is thought to be maintained primarily by the vasodilatory effect of PGE, both in utero and in prematurely born infants, and lung is a major source of PGE, in fetuses and neonates. 15-Hydroxy-prostaglandin dehydrogenase (15-PGDH) catalyzes the initial reaction in converting biologically active PGE, to its inactive analogue, 15-keto-PGE2. In the present study, effect of prenatal dexamethasone treatment on the activity of fetal rat lung 15-PGDH was studied at 20, 21 and 22 days of gestation.

Activity of fetal lung 15-PGDH more than doubled from 20 to 22 days of gestation. Dexamethasone treatment at 0.4 mg/kg and 0.8 mg/kg significantly increased the activity of 15-PGDH in both 20- and 21-day fetuses but had no effect on 2 22-day fetuses. We speculate that the clinical observation that prenatal glucocorticoid treatment reduces the incidence of patent ductus arteriosus in premature infants say in part be due to the stimulatory effect of glucocorticoid-on the activity of 15-PGDH in fetal and neonatal lung and possibly other organs.

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