Human pulmonary vascular response to 4 h of hypercapnia and hypocapnia measured using Doppler echo cardiography
Human pulmonary vascular response to 4 h of hypercapnia and hypocapnia measured using Doppler echo cardiography
复制标题
DOI：
10.1152/japplphysiol.00890.2002
复制
发表时间：
2003-04-01
影响因子：
3.3
通讯作者：
Robbins, PA
中科院分区：
文献类型：
--
作者：
Balanos, GM;Talbot, NP;Robbins, PA
在动物实验中，过度睡眠已被证明会诱发肺动脉高压。本研究测量了人肺血管对持续（4 h）高碳酸血症和低碳酸血症反应的敏感性和时程。12名志愿者接受了三种方案：1）4小时的正常氧（潮气末Po-2 = 100 Torr）高碳酸血症（潮气末PCo 2比正常值高10 Torr），随后恢复2小时的正常氧高碳酸血症; 2）4小时的正常氧低碳酸血症（潮气末PCo 2比正常值低10 Torr），随后恢复2小时; 3）6小时的空气呼吸（对照）。通过多普勒超声心动图在收缩期通过最大三尖瓣压力梯度在0.5至1小时的时间间隔评估肺血管阻力。结果显示，在刺激的开始或偏移后1-2小时内压力梯度的渐进变化，以及潮气末PCo 2中每Torr变化的压力梯度变化为0.6至I Torr的灵敏度。人体肺循环对PCo 2变化的反应比通常假设的时间过程更慢，灵敏度更高。正常肺循环中的血管张力是相当大的。
Hypereapnia has been shown in animal experiments to induce pulmonary hypertension. This study measured the sensitivity and time course of the human pulmonary vascular response to sustained (4 h) hypercapnia and hypocapnia. Twelve volunteers undertook three protocols: 1) 4-h euoxic (end-tidal Po-2 = 100 Torr) hypercapnia (end-tidal PCo2 was 10 Torr above normal), followed by 2 h of recovery with euoxic eucapnia; 2) 4-h euoxic hypocapnia (end-tidal PCo2 was 10 Torr below normal) followed by 2 h of recovery; and 3) 6-h air breathing (control). Pulmonary vascular resistance was assessed at 0.5- to 1-h intervals by using Doppler echocardiography via the maximum tricuspid pressure gradient during systole. Results show progressive changes in pressure gradient over 1-2 h after the onset or offset of the stimuli, and sensitivities of 0.6 to I Torr change in pressure gradient per Torr change in end-tidal PCo2. The human pulmonary circulatory response to changes in PCo2 has a slower time course and greater sensitivity than is commonly assumed. Vascular tone in the normal pulmonary circulation is substantial.