Palkovits Stefan, Lasta Michael, Told Reinhard, Schmidl Doreen, Boltz Agnes, Napora Katarzyna J, Werkmeister René M, Popa-Cherecheanu Alina, Garhöfer Gerhard, Schmetterer Leopold
Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria.
Invest Ophthalmol Vis Sci. 2014 Jul 11;55(8):4707-13. doi: 10.1167/iovs.14-14593.
To characterize retinal metabolism during normoxia and hyperoxia in healthy subjects.
Forty-six healthy subjects were included in the present study, and data of 41 subjects could be evaluated. Retinal vessel diameters, as well as oxygen saturation in arteries and veins, were measured using the Dynamic Vessel Analyzer. In addition, retinal venous blood velocity was measured using bidirectional laser Doppler velocimetry, retinal blood flow was calculated, and oxygen and carbon dioxide partial pressures were measured from arterialized capillary blood from the earlobe. Measurements were done during normoxia and during 100% oxygen breathing.
Systemic hyperoxia caused a significant decrease in retinal venous diameter (-13.0% ± 4.5%) and arterial diameter (-12.1% ± 4.0%), in retinal blood velocity (-43.4% ± 7.7%), and in retinal blood flow (-57.0% ± 5.7%) (P < 0.001 for all). Oxygen saturation increased in retinal arteries (+4.4% ± 2.3%) and in retinal veins (+19.6% ± 6.2%), but the arteriovenous oxygen content difference significantly decreased (-29.4% ± 19.5%) (P < 0.001 for all). Blood oxygen tension in arterialized blood showed a pronounced increase from 90.2 ± 7.7 to 371.3 ± 92.7 mm Hg (P < 0.001). Calculated oxygen extraction in the eye decreased by as much as 62.5% ± 9.5% (P < 0.001).
Our data are compatible with the hypothesis that during 100% oxygen breathing a large amount of oxygen, consumed by the inner retina, comes from the choroid, which is supported by previous animal data. Interpretation of oxygen saturation data in retinal arteries and veins without quantifying blood flow is difficult. (ClinicalTrials.gov number, NCT01692821.).
描述健康受试者在常氧和高氧状态下的视网膜代谢情况。
本研究纳入了46名健康受试者，其中41名受试者的数据可进行评估。使用动态血管分析仪测量视网膜血管直径以及动脉和静脉中的氧饱和度。此外，使用双向激光多普勒测速仪测量视网膜静脉血流速度，计算视网膜血流量，并从耳垂的动脉化毛细血管血中测量氧分压和二氧化碳分压。测量在常氧状态下以及吸入100%氧气时进行。
全身性高氧导致视网膜静脉直径显著减小（-13.0%±4.5%）、动脉直径显著减小（-12.1%±4.0%）、视网膜血流速度显著降低（-43.4%±7.7%）以及视网膜血流量显著减少（-57.0%±5.7%）（所有P<0.001）。视网膜动脉中的氧饱和度升高（+4.4%±2.3%），视网膜静脉中的氧饱和度升高（+19.6%±6.2%），但动静脉氧含量差显著降低（-29.4%±19.5%）（所有P<0.001）。动脉化血液中的血氧张力从90.2±7.7显著升高至371.3±92.7mmHg（P<0.001）。眼部计算得出的氧摄取量降低了多达62.5%±9.5%（P<0.001）。
我们的数据与以下假设相符，即在吸入100%氧气期间，视网膜内层消耗的大量氧气来自脉络膜，先前的动物数据支持这一观点。在不量化血流的情况下解释视网膜动脉和静脉中的氧饱和度数据较为困难。（ClinicalTrials.gov编号，NCT01692821.）
