Berenji Ardestani Simin, Matchkov Vladimir V, Hansen Kasper, Jespersen Nichlas Riise, Pedersen Michael, Eftedal Ingrid
MEMBRANES, Department of Biomedicine, Faculty of Health, Aarhus University, Aarhus, Denmark.
Department of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, NTNU Norwegian University of Science and Technology, Trondheim, Norway.
Front Physiol. 2020 Dec 23;11:611208. doi: 10.3389/fphys.2020.611208. eCollection 2020.
The average age of the diving population is rising, and the risk of atherosclerosis and cardiovascular disease in divers are accordingly increasing. It is an open question whether this risk is altered by diving . In this study, we examined the effect of 7-weeks simulated diving on endothelial function and mitochondrial respiration in atherosclerosis-prone rats.
Twenty-four male ApoE knockout (KO) rats (9-weeks-old) were fed a Western diet for 8 weeks before 12 rats were exposed to simulated heliox dry-diving in a pressure chamber (600 kPa for 60 min, decompression of 50 kPa/min). The rats were dived twice-weekly for 7 weeks, resulting in a total of 14 dives. The remaining 12 non-diving rats served as controls. Endothelial function of the pulmonary and mesenteric arteries was examined using an isometric myograph. Mitochondrial respiration in cardiac muscle tissues was measured using high-resolution respirometry.
Both ApoE KO diving and non-diving rats showed changes in endothelial function at the end of the intervention, but the extent of these changes was larger in the diving group. Altered nitric oxide signaling was primarily involved in these changes. Mitochondrial respiration was unaltered. In this pro-atherosclerotic rat model of cardiovascular changes, extensive diving appeared to aggravate endothelial dysfunction rather than promote adaptation to oxidative stress.
潜水人群的平均年龄在上升，潜水员患动脉粥样硬化和心血管疾病的风险也相应增加。潜水是否会改变这种风险仍是一个悬而未决的问题。在本研究中，我们检测了7周模拟潜水对易患动脉粥样硬化大鼠内皮功能和线粒体呼吸的影响。
24只雄性载脂蛋白E基因敲除（KO）大鼠（9周龄）在接受西式饮食8周后，将12只大鼠置于压力舱中进行模拟氦氧混合气干式潜水（600 kPa，持续60分钟，减压速度为50 kPa/分钟）。大鼠每周潜水两次，共7周，总计潜水14次。其余12只非潜水大鼠作为对照。使用等长肌张力测定仪检测肺和肠系膜动脉的内皮功能。使用高分辨率呼吸测定法测量心肌组织中的线粒体呼吸。
干预结束时，载脂蛋白E基因敲除的潜水大鼠和非潜水大鼠的内皮功能均发生了变化，但潜水组的变化程度更大。一氧化氮信号改变主要参与了这些变化。线粒体呼吸未改变。在这个心血管变化的动脉粥样硬化前期大鼠模型中，大量潜水似乎加剧了内皮功能障碍，而不是促进对氧化应激的适应。
