Brett S J, Simon J, Gibbs R, Pepper J R, Evans T W
Unit of Critical Care, National Heart and Lung Institute, London, UK.
Thorax. 1996 Jan;51(1):89-91. doi: 10.1136/thx.51.1.89.
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).
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.
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).
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.
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。
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。
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)。
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。