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本文引用的文献

1
Pulmonary hypertension in extremely low birth weight infants: characteristics and outcomes.极低出生体重儿的肺动脉高压:特征与结局。
World J Pediatr. 2014 Feb;10(1):46-52. doi: 10.1007/s12519-014-0464-2. Epub 2014 Jan 25.
2
Molecular mechanisms of endothelial NO synthase uncoupling.内皮型一氧化氮合酶解偶联的分子机制。
Curr Pharm Des. 2014;20(22):3548-53. doi: 10.2174/13816128113196660746.
3
Predictors of bronchopulmonary dysplasia and pulmonary hypertension in newborn children.新生儿支气管肺发育不良和肺动脉高压的预测因素
Dan Med J. 2013 Aug;60(8):A4688.
4
Nitric oxide deficiency and endothelial dysfunction in pulmonary arterial hypertension.肺动脉高压中的一氧化氮缺乏和内皮功能障碍。
Am J Respir Crit Care Med. 2013 Sep 15;188(6):639-46. doi: 10.1164/rccm.201304-0686PP.
5
Pulmonary vascular disease in bronchopulmonary dysplasia: pulmonary hypertension and beyond.支气管肺发育不良中的肺血管疾病:肺动脉高压及其他。
Curr Opin Pediatr. 2013 Jun;25(3):329-37. doi: 10.1097/MOP.0b013e328360a3f6.
6
Pulmonary hypertension in bronchopulmonary dysplasia.支气管肺发育不良中的肺动脉高压。
Semin Perinatol. 2013 Apr;37(2):124-31. doi: 10.1053/j.semperi.2013.01.009.
7
Fetal growth restriction and pulmonary hypertension in premature infants with bronchopulmonary dysplasia.支气管肺发育不良早产儿的胎儿生长受限和肺动脉高压。
J Perinatol. 2013 Jul;33(7):553-7. doi: 10.1038/jp.2012.164. Epub 2013 Jan 17.
8
Frontiers in pulmonary hypertension in infants and children with bronchopulmonary dysplasia.支气管肺发育不良婴儿和儿童的肺动脉高压的前沿问题。
Pediatr Pulmonol. 2012 Nov;47(11):1042-53. doi: 10.1002/ppul.22609. Epub 2012 Jul 6.
9
Prospective analysis of pulmonary hypertension in extremely low birth weight infants.极低出生体重儿肺动脉高压的前瞻性分析。
Pediatrics. 2012 Mar;129(3):e682-9. doi: 10.1542/peds.2011-1827. Epub 2012 Feb 6.
10
Risk factors for pulmonary artery hypertension in preterm infants with moderate or severe bronchopulmonary dysplasia.早产儿中伴有中重度支气管肺发育不良的肺动脉高压的危险因素。
Neonatology. 2012;101(1):40-6. doi: 10.1159/000327891. Epub 2011 Jul 26.

支气管肺发育不良相关肺动脉高压新生儿的血浆不对称二甲基精氨酸水平升高。

Plasma asymmetric dimethylarginine levels are increased in neonates with bronchopulmonary dysplasia-associated pulmonary hypertension.

作者信息

Trittmann Jennifer K, Peterson Eric, Rogers Lynette K, Chen Bernadette, Backes Carl H, Klebanoff Mark A, Nelin Leif D

机构信息

The Research Institute at Nationwide Children's Hospital, Columbus, OH; Pulmonary Hypertension Group, Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, Columbus, OH; Department of Pediatrics, The Ohio State University, Columbus, OH.

Department of Pediatrics, The Ohio State University, Columbus, OH.

出版信息

J Pediatr. 2015 Feb;166(2):230-3. doi: 10.1016/j.jpeds.2014.09.004. Epub 2014 Oct 11.

DOI:10.1016/j.jpeds.2014.09.004
PMID:25311706
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4308509/
Abstract

OBJECTIVE

To test the hypothesis that levels of the endogenous inhibitor of nitric oxide production, asymmetric dimethylarginine (ADMA), would be greater in preterm infants with bronchopulmonary dysplasia (BPD)-associated pulmonary hypertension (PH) than in infants with BPD alone.

STUDY DESIGN

A case-control study of 23 patients with both BPD and PH (cases) and 95 patients with BPD but no evidence of PH (controls). Levels of ADMA were compared between cases and controls by t test.

RESULTS

Patients with both BPD and PH had greater plasma levels of ADMA than patients with BPD alone (P = .04). In samples drawn before 28 days of life, greater levels of ADMA were again found in cases compared with controls (P = .02). The plasma arginine-to-ADMA ratio was lower in cases than in controls (P = .03), suggesting a greater likelihood of inhibition of nitric oxide production in patients with both BPD and PH than in patients with BPD alone.

CONCLUSION

In this neonatal BPD cohort, ADMA levels are increased in patients with BPD who develop PH. We speculate that ADMA may be both a biomarker and a potential therapeutic target for preterm infants with BPD-associated PH.

摘要

目的

检验如下假设,即与仅患支气管肺发育不良(BPD)的婴儿相比,患有与BPD相关的肺动脉高压(PH)的早产儿体内一氧化氮生成的内源性抑制剂非对称二甲基精氨酸(ADMA)水平更高。

研究设计

一项病例对照研究,纳入23例同时患有BPD和PH的患者(病例组)以及95例患有BPD但无PH证据的患者(对照组)。通过t检验比较病例组和对照组的ADMA水平。

结果

同时患有BPD和PH的患者血浆ADMA水平高于仅患BPD的患者(P = 0.04)。在出生28天前采集的样本中,病例组的ADMA水平再次高于对照组(P = 0.02)。病例组的血浆精氨酸与ADMA比值低于对照组(P = 0.03),这表明与仅患BPD的患者相比,同时患有BPD和PH的患者抑制一氧化氮生成的可能性更大。

结论

在这个新生儿BPD队列中,发生PH的BPD患者的ADMA水平升高。我们推测,ADMA可能既是患有BPD相关PH的早产儿的生物标志物,也是潜在的治疗靶点。