Frøbert Ole, Moesgaard Jacob, Toft Egon, Poulsen Steen Hvitfeldt, Søgaard Peter
Department of Cardiology, Center for Cardiovascular Research, Aalborg Hospital, Aarhus University Hospital, Denmark.
Cardiovasc Ultrasound. 2004 Nov 2;2:22. doi: 10.1186/1476-7120-2-22.
Low O2 tension dilates coronary arteries and high O2 tension is a coronary vasoconstrictor but reports on O2-dependent effects on ventricular performance diverge. Yet oxygen supplementation remains first line treatment in cardiovascular disease. We hypothesized that hypoxia improves and hyperoxia worsens myocardial performance.
Seven male volunteers (mean age 38 +/- 3 years) were examined with echocardiography at respiratory equilibrium during: 1) normoxia (approximately 21% O2, 79% N2), 2) while inhaling a hypoxic gas mixture (approximately 11% O2, 89% N2), and 3) while inhaling 100% O2. Tissue Doppler recordings were acquired in the apical 4-chamber, 2-chamber, and long-axis views. Strain rate and tissue tracking displacement analyses were carried out in each segment of the 16-segment left ventricular model and in the basal, middle and apical portions of the right ventricle.
Heart rate increased with hypoxia (68 +/- 4 bpm at normoxia vs. 79 +/- 5 bpm, P < 0.001) and decreased with hyperoxia (59 +/- 5 bpm, P < 0.001 vs. normoxia). Hypoxia increased strain rate in four left ventricular segments and global systolic contraction amplitude was increased (normoxia: 9.76 +/- 0.41 vs hypoxia: 10.87 +/- 0.42, P < 0.001). Tissue tracking displacement was reduced in the right ventricular segments and tricuspid regurgitation increased with hypoxia (7.5 +/- 1.9 mmHg vs. 33.5 +/- 1.8 mmHg, P < 0.001). The TEI index and E/E' did not change with hypoxia. Hyperoxia reduced strain rate in 10 left ventricular segments, global systolic contraction amplitude was decreased (8.83 +/- 0.38, P < 0.001 vs. normoxia) while right ventricular function was unchanged. The spectral and tissue Doppler TEI indexes were significantly increased but E/E' did not change with hyperoxia.
Hypoxia improves and hyperoxia worsens systolic myocardial performance in healthy male volunteers. Tissue Doppler measures of diastolic function are unaffected by hypoxia/hyperoxia which support that the changes in myocardial performance are secondary to changes in vascular tone. It remains to be settled whether oxygen therapy to patients with heart disease is a consistent rational treatment.
低氧张力可使冠状动脉扩张，高氧张力则是冠状动脉收缩剂，但关于氧对心室功能影响的报道却存在分歧。然而，补充氧气仍是心血管疾病的一线治疗方法。我们推测低氧可改善心肌功能，而高氧则会使其恶化。
对7名男性志愿者（平均年龄38±3岁）在呼吸平衡状态下进行超声心动图检查，检查期间分别为：1）常氧状态（约21%氧气，79%氮气）；2）吸入低氧混合气体（约11%氧气，89%氮气）；3）吸入100%氧气。在心尖四腔心、两腔心和长轴视图下进行组织多普勒记录。在16节段左心室模型的每个节段以及右心室的基底、中间和心尖部分进行应变率和组织追踪位移分析。
低氧时心率增加（常氧时为68±4次/分，低氧时为79±5次/分，P<0.001），高氧时心率降低（59±5次/分，与常氧相比P<0.001）。低氧使四个左心室节段的应变率增加，整体收缩期收缩幅度增大（常氧：9.76±0.41，低氧：10.87±0.42，P<0.001）。右心室节段的组织追踪位移减小，低氧时三尖瓣反流增加（7.5±1.9 mmHg对33.5±1.8 mmHg，P<0.001）。低氧时TEI指数和E/E'未发生变化。高氧使10个左心室节段的应变率降低，整体收缩期收缩幅度减小（8.83±0.38，与常氧相比P<0.001），而右心室功能未改变。频谱和组织多普勒TEI指数显著增加，但高氧时E/E'未发生变化。
在健康男性志愿者中，低氧可改善心肌收缩功能，高氧则会使其恶化。组织多普勒测量的舒张功能不受低氧/高氧的影响，这支持心肌功能的变化继发于血管张力的变化。心脏病患者的氧疗是否始终是合理的治疗方法仍有待确定。
