首页> 外文期刊>Journal of Perinatal Medicine >Endothelin-1 levels in infants with pulmonary hypertension receiving extracorporeal membrane oxygenation.
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Endothelin-1 levels in infants with pulmonary hypertension receiving extracorporeal membrane oxygenation.

机译:接受体外膜氧合的肺动脉高压婴儿的内皮素-1水平。

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摘要

We studied the possibility of an etiological role for endothelin-1 (ET-1) in the development of persistent pulmonary hypertension of the newborn (PPHN). Ten infants with severe PPHN requiring extracorporeal membrane oxygenation (ECMO) were studied. Pre and post pulmonary blood samples were obtained on commencing ECMO and on recovery. The samples were analyzed by radio-immunoassay. The infants with PPHN requiring ECMO had a significantly higher mean ET-1 concentration (21.1 pmol/l, S. D. 3.59) than a group of healthy controls (16.6 pmol/l, S. D. 4.44); however 8 of our 10 infants had individual ET-1 levels within our reference range for healthy newborns. Pre and post pulmonary ET-1 levels did not differ significantly and there was no evidence of a decline in ET-1 levels with resolution of PPHN. Pulmonary overproduction of ET-1 does not appear to be the cause of PPHN, although the endothelin system may still play a role in the pathophysiology of PPHN, probably mediated through changes in receptor expression.
机译:我们研究了内皮素-1(ET-1)在新生儿持续性肺动脉高压(PPHN)发展中的病因作用的可能性。研究了10例需要体外膜氧合(ECMO)的严重PPHN婴儿。开始ECMO并恢复时获取肺部血样前后。通过放射免疫测定法分析样品。需要ECMO的PPHN婴儿的平均ET-1浓度(21.1 pmol / l,S。D. 3.59)比一组健康对照组(16.6 pmol / l,S。D. 4.44)高得多。然而,在我们的10名婴儿中,有8名的ET-1水平在健康新生儿的参考范围内。肺ET-1前后的水平无显着差异,并且没有证据表明随着PPHN的分解,ET-1水平下降。尽管内皮素系统可能仍在PPHN的病理生理中起作用,可能是通过受体表达的改变介导的,但ET-1的肺过度产生似乎不是PPHN的原因。

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