Bak Z, Sjöberg F, Rousseau A, Steinvall I, Janerot-Sjoberg B
Department of Anesthesia and Intensive Care, and Departments of Hand and Plastic Surgery and Burn Intensive Care, University Hospital, Linköping, Sweden.
Acta Physiol (Oxf). 2007 Sep;191(1):15-24. doi: 10.1111/j.1748-1716.2007.01710.x. Epub 2007 May 17.
The aim of the study was to examine the central and peripheral cardiovascular adaptation and its coupling during increasing levels of hyperoxaemia. We hypothesized a dose-related effect of hyperoxaemia on left ventricular performance and the vascular properties of the arterial tree.
Oscillometrically calibrated arterial subclavian pulse trace data were combined with echocardiographic recordings to obtain non-invasive estimates of left ventricular volumes, aortic root pressure and flow data. For complementary vascular parameters and control purposes whole-body impedance cardiography was applied. In nine (seven males) supine, resting healthy volunteers, aged 23-48 years, data was collected after 15 min of air breathing and at increasing transcutaneous oxygen tensions (20, 40 and 60 kPa), accomplished by a two group, random order and blinded hyperoxemic protocol.
Left ventricular stroke volume [86 +/- 13 to 75 +/- 9 mL (mean +/- SD)] and end-diastolic area (19.3 +/- 4.4 to 16.8 +/- 4.3 cm(2)) declined (P < 0.05), and showed a linear, negative dose-response relationship to increasing arterial oxygen levels in a regression model. Peripheral resistance and characteristic impedance increased in a similar manner. Heart rate, left ventricular fractional area change, end-systolic area, mean arterial pressure, arterial compliance or carbon dioxide levels did not change.
There is a linear dose-response relationship between arterial oxygen and cardiovascular parameters when the systemic oxygen tension increases above normal. A direct effect of supplemental oxygen on the vessels may therefore not be excluded. Proximal aortic and peripheral resistance increases from hyperoxaemia, but a decrease of venous return implies extra cardiac blood-pooling and compensatory relaxation of the capacitance vessels.
本研究旨在探讨高氧血症程度增加时的中枢和外周心血管适应性及其耦合关系。我们假设高氧血症对左心室功能和动脉树血管特性存在剂量相关效应。
将经振荡法校准的锁骨下动脉脉搏轨迹数据与超声心动图记录相结合,以获得左心室容积、主动脉根部压力和血流数据的无创估计值。为获取补充性血管参数并用于对照,应用了全身阻抗心动图。在9名(7名男性)年龄在23 - 48岁的仰卧、静息健康志愿者中,在呼吸空气15分钟后以及经皮氧分压升高(20、40和60 kPa)时收集数据,采用两组随机顺序且双盲的高氧方案。
左心室每搏输出量[86 ± 13至75 ± 9 mL(均值 ± 标准差)]和舒张末期面积(19.3 ± 4.4至16.8 ± 4.3 cm²)下降(P < 0.05),并且在回归模型中显示出与动脉氧水平升高呈线性负剂量反应关系。外周阻力和特性阻抗以类似方式增加。心率、左心室面积变化分数、收缩末期面积、平均动脉压、动脉顺应性或二氧化碳水平未发生变化。
当全身氧分压高于正常水平时,动脉氧与心血管参数之间存在线性剂量反应关系。因此,不能排除补充氧气对血管的直接作用。高氧血症导致近端主动脉和外周阻力增加,但静脉回流量减少意味着心外血液蓄积和容量血管的代偿性舒张。