Brubakk A O, Duplancic D, Valic Z, Palada I, Obad A, Bakovic D, Wisloff U, Dujic Z
Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.
J Physiol. 2005 Aug 1;566(Pt 3):901-6. doi: 10.1113/jphysiol.2005.089862. Epub 2005 Jun 16.
During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 +/- 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min(-1) with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 +/- 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow-mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 +/- 0.7 to 4.8 +/- 0.8 mm (mean +/- s.d.) and a significant reduction of FMD from 9.2 +/- 6.9 to 5.0 +/- 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 +/- 0.3 mm to 4.7 +/- 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine-induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 +/- 0.4 mm and 7.7 +/- 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving.
在潜水减压期间及之后,经常会在右心室流出道观察到气泡。多项研究已证明,这些气泡可导致肺动脉内皮功能障碍,但关于潜水对动脉内皮功能影响的数据尚不存在。本研究调查了潜水或吸氧是否会影响人体的动脉内皮功能。共有21名潜水员参与了本研究。9名健康且经验丰富的男性潜水员,平均年龄为31±5岁,在高压舱内以100 kPa/min(-1)的速率呼吸空气加压至280 kPa,并在该压力下停留80分钟。减压过程中的上升速率为9 kPa/min(-1),在130 kPa处停留7分钟(美国海军程序)。另一组5名经验丰富的男性潜水员(31±6岁)吸入60%的氧气(相当于280 kPa时空气中的氧分压)80分钟。在暴露前后,两组均通过超声测量肱动脉的血流介导的血管舒张(FMD)来评估内皮功能。将结果与一组7名从未潜水的同龄健康个体的数据进行比较。潜水产生的血管气泡较少,但观察到动脉直径显著增加,从4.5±0.7毫米增加到4.8±0.8毫米(平均值±标准差),同时FMD显著降低,从9.2±6.9%降至5.0±6.7%,这表明内皮功能降低。在吸氧组中,动脉直径从4.4±0.3毫米显著增加到4.7±0.3毫米,而FMD显示出不显著的下降。吸氧并未显著降低硝酸甘油诱导的血管舒张。在正常对照组中,动脉直径和FMD分别为4.1±0.4毫米和7.7±0.28%。本研究表明,潜水可导致人体急性动脉内皮功能障碍,并且吸氧在恢复呼吸空气后会增加动脉直径。需要进一步研究以确定这些机制是否与潜水后的组织损伤有关。