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一氧化氮合酶在患有肺动脉高压和先天性心脏病的婴儿和儿童中的作用。

Nitric oxide synthases in infants and children with pulmonary hypertension and congenital heart disease.

机构信息

Neonatology and Pediatric Intensive Care Medicine, Department of General Pediatrics, Heinrich-Heine-University, Duesseldorf, Germany.

出版信息

Respir Res. 2009 Nov 13;10(1):110. doi: 10.1186/1465-9921-10-110.

DOI:10.1186/1465-9921-10-110
PMID:19912632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2780406/
Abstract

RATIONALE

Nitric oxide is an important regulator of vascular tone in the pulmonary circulation. Surgical correction of congenital heart disease limits pulmonary hypertension to a brief period.

OBJECTIVES

The study has measured expression of endothelial (eNOS), inducible (iNOS), and neuronal nitric oxide synthase (nNOS) in the lungs from biopsies of infants with pulmonary hypertension secondary to cardiac abnormalities (n = 26), compared to a control group who did not have pulmonary or cardiac disease (n = 8).

METHODS

eNOS, iNOS and nNOS were identified by immunohistochemistry and quantified in specific cell types.

MEASUREMENTS AND MAIN RESULTS

Significant increases of eNOS and iNOS staining were found in pulmonary vascular endothelial cells of patients with congenital heart disease compared to control infants. These changes were confined to endothelial cells and not present in other cell types. Patients who strongly expressed eNOS also had strong expression of iNOS.

CONCLUSION

Upregulation of eNOS and iNOS occurs at an early stage of pulmonary hypertension, and may be a compensatory mechanism limiting the rise in pulmonary artery pressure.

摘要

原理

一氧化氮是肺循环中血管张力的重要调节剂。先天性心脏病的手术矫正将肺动脉高压限制在很短的时间内。

目的

本研究通过免疫组织化学方法检测了 26 例因心脏异常而导致肺动脉高压的婴儿肺组织中内皮型(eNOS)、诱导型(iNOS)和神经元型一氧化氮合酶(nNOS)的表达,并与无肺部或心脏疾病的对照组(n=8)进行了比较。

方法

通过免疫组织化学方法鉴定 eNOS、iNOS 和 nNOS,并对特定细胞类型进行定量。

测量和主要结果

与对照组婴儿相比,先天性心脏病患者的肺血管内皮细胞中发现 eNOS 和 iNOS 染色明显增加。这些变化仅限于内皮细胞,而不存在于其他细胞类型中。强烈表达 eNOS 的患者也强烈表达 iNOS。

结论

eNOS 和 iNOS 的上调发生在肺动脉高压的早期,可能是一种限制肺动脉压升高的代偿机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274d/2780406/f632b155e283/1465-9921-10-110-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274d/2780406/22ad18b96cb3/1465-9921-10-110-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274d/2780406/f632b155e283/1465-9921-10-110-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274d/2780406/22ad18b96cb3/1465-9921-10-110-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274d/2780406/f632b155e283/1465-9921-10-110-2.jpg

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Diminished NO release in chronic hypoxic human endothelial cells.慢性缺氧的人内皮细胞中一氧化氮释放减少。
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