Suppr超能文献

原发性肺动脉高压患者内皮依赖性肺血管舒张功能受损。

Impairment of endothelium-dependent pulmonary vasodilation in patients with primary pulmonary hypertension.

作者信息

Brett S J, Simon J, Gibbs R, Pepper J R, Evans T W

机构信息

Unit of Critical Care, National Heart and Lung Institute, London, UK.

出版信息

Thorax. 1996 Jan;51(1):89-91. doi: 10.1136/thx.51.1.89.

Abstract

BACKGROUND

Pulmonary vascular tone may be modulated by endothelium-derived vasoactive mediators. Endothelial dysfunction is thought to occur in primary pulmonary hypertension. The aim of this study was to evaluate the vascular responses of patients with severe primary pulmonary hypertension to endothelium-dependent vasodilators (for example, substance P) and non-endothelium-dependent vaasodilators (for example, adenosine).

METHODS

Six patients with primary pulmonary hypertension (mean (SE) systolic, diastolic, and pulmonary artery pressures 91.1 (7), 45.2 (3), and 62 (4.2) mm Hg, respectively, and baseline total pulmonary vascular resistance (TPVR) 1949 (164) dynes.s.cm-5) underwent sequential infusions of substance P (5-100 pmol/min) and adenosine (5-50 micrograms/kg/min) in random order. Pulmonary and systemic haemodynamics were monitored by indwelling radial and pulmonary arterial catheters.

RESULTS

Substance P caused a marked fall in systemic vascular resistance (SVR) but minimal pulmonary vasodilation (mean maximal percentage change from baseline in TPVR:SVR ratio 27.85 (6.5)%, p < 0.01). Adenosine caused TPVR to fall, but resulted in no change in SVR (mean maximum percentage change from baseline in TPVR:SVR ratio -9.85 (3.5)%, p < 0.05).

CONCLUSION

Endothelium-dependent vasodilation is deficient in the pulmonary circulation of patients with primary pulmonary hypertension and may contribute to the abnormalities of pulmonary vascular tone and reactivity seen in that condition.

摘要

背景

肺血管张力可能受内皮源性血管活性介质调节。内皮功能障碍被认为发生于原发性肺动脉高压。本研究旨在评估重度原发性肺动脉高压患者对内皮依赖性血管扩张剂(如P物质)和非内皮依赖性血管扩张剂(如腺苷)的血管反应。

方法

6例原发性肺动脉高压患者(平均(标准误)收缩压、舒张压和肺动脉压分别为91.1(7)、45.2(3)和62(4.2)mmHg,基线总肺血管阻力(TPVR)为1949(164)达因·秒·厘米⁻⁵),按随机顺序依次输注P物质(5 - 100 pmol/min)和腺苷(5 - 50μg/kg/min)。通过留置桡动脉和肺动脉导管监测肺和全身血流动力学。

结果

P物质使全身血管阻力(SVR)显著下降,但肺血管扩张极小(TPVR:SVR比值相对于基线的平均最大百分比变化为27.85(6.5)%,p < 0.01)。腺苷使TPVR下降,但SVR无变化(TPVR:SVR比值相对于基线的平均最大百分比变化为 - 9.85(3.5)%,p < 0.05)。

结论

原发性肺动脉高压患者肺循环中内皮依赖性血管舒张功能不足,可能导致该疾病中所见的肺血管张力和反应性异常。

相似文献

9
Systemic and pulmonary hypertension after abrupt cessation of prostacyclin: role of thromboxane A2.
J Appl Physiol (1985). 1996 Jan;80(1):191-7. doi: 10.1152/jappl.1996.80.1.191.

本文引用的文献

1
Primary pulmonary hypertension.原发性肺动脉高压
Prog Cardiovasc Dis. 1988 Nov-Dec;31(3):205-38. doi: 10.1016/0033-0620(88)90016-3.
5
Inhaled nitric oxide as a cause of selective pulmonary vasodilatation in pulmonary hypertension.
Lancet. 1991 Nov 9;338(8776):1173-4. doi: 10.1016/0140-6736(91)92033-x.
8
Endothelial dysfunction in pulmonary hypertension.
N Engl J Med. 1992 Jul 9;327(2):117-9. doi: 10.1056/NEJM199207093270209.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验