关键词: acute pulmonary edema breath-hold diving nitric oxide

Mesh : Humans Male Diving / physiology adverse effects Adult Altitude Breath Holding Young Adult Echocardiography, Doppler Hypoxia / physiopathology Middle Aged Adolescent Lung / physiopathology diagnostic imaging blood supply Pulmonary Edema / etiology physiopathology diagnostic imaging Arterial Pressure / physiology Oxygen Saturation / physiology Nitric Oxide / metabolism Blood Pressure / physiology Hemoglobins / analysis

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Abstract:
Hypoxia, centralization of blood in pulmonary vessels, and increased cardiac output during physical exertion are the pathogenetic pathways of acute pulmonary edema observed during exposure to extraordinary environments. This study aimed to evaluate the effects of breath-hold diving at altitude, which exposes simultaneously to several of the stimuli mentioned above. To this aim, 11 healthy male experienced divers (age 18-52y) were evaluated (by Doppler echocardiography, lung echography to evaluate ultrasound lung B-lines (BL), hemoglobin saturation, arterial blood pressure, fractional NO (Nitrous Oxide) exhalation in basal condition (altitude 300m asl), at altitude (2507m asl) and after breath-hold diving at altitude. A significant increase in E/e\' ratio (a Doppler-echocardiographic index of left atrial pressure) was observed at altitude, with no further change after the diving session. The number of BL significantly increased after diving at altitude as compared to basal conditions. Finally, fractional exhaled nitrous oxide was significantly reduced by altitude; no further change was observed after diving. Our results suggest that exposure to hypoxia may increase left ventricular filling pressure and, in turn, pulmonary capillary pressure. Breath-hold diving at altitude may contribute to interstitial edema (as evaluated by BL score), possibly because of physical efforts made during a diving session. The reduction of exhaled nitrous oxide at altitude confirms previous reports of nitrous oxide reduction after repeated exposure to hypoxic stimuli. This finding should be further investigated since reduced nitrous oxide production in hypoxic conditions has been reported in subjects prone to high-altitude pulmonary edema.
摘要:
缺氧,血液集中在肺血管中,体力消耗期间心输出量增加是暴露于特殊环境期间观察到的急性肺水肿的发病途径。本研究旨在评估高空屏气潜水的效果,同时暴露于上述几种刺激。为了这个目标,对11名健康的有经验的男性潜水员(年龄18-52岁)进行了评估(通过多普勒超声心动图,肺回波描记术评估超声肺B线(BL),血红蛋白饱和度,动脉血压,在基础条件下(海拔300masl),在海拔高度(2507masl)和在海拔高度屏气潜水后。在海拔高度观察到E/e比值(左心房压力的多普勒超声心动图指数)显著增加,潜水后没有进一步的变化。与基础条件相比,在高空潜水后BL的数量显着增加。最后,呼出气一氧化二氮的分数随海拔高度显著降低;潜水后未观察到进一步变化.我们的结果表明,暴露于缺氧可能会增加左心室充盈压,反过来,肺毛细血管压.高空屏气潜水可能导致间质性水肿(通过BL评分评估)。可能是由于在潜水期间所做的身体努力。高海拔地区呼出气一氧化二氮的减少证实了先前关于反复暴露于低氧刺激后一氧化二氮减少的报道。应进一步研究这一发现,因为据报道,在容易发生高原肺水肿的受试者中,低氧条件下一氧化二氮的产生减少。
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