102 research outputs found

    Renin-Angiotensin-Aldosterone System Is Not Involved in the Arterial Stiffening Induced by Acute and Prolonged Exposure to High Altitude

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    This randomized, double-blind, placebo-controlled study was designed to explore the effects of exposure to very high altitude hypoxia on vascular wall properties and to clarify the role of renin-angiotensin-aldosterone system inhibition on these vascular changes. Forty-seven healthy subjects were included in this study: 22 randomized to telmisartan (age, 40.3±10.8 years; 7 women) and 25 to placebo (age, 39.3±9.8 years; 7 women). Tests were performed at sea level, pre- and post-treatment, during acute exposure to 3400 and 5400-m altitude (Mt. Everest Base Camp), and after 2 weeks, at 5400 m. The effects of hypobaric hypoxia on mechanical properties of large arteries were assessed by applanation tonometry, measuring carotid-femoral pulse wave velocity, analyzing arterial pulse waveforms, and evaluating subendocardial oxygen supply/demand index. No differences in hemodynamic changes during acute and prolonged exposure to 5400-m altitude were found between telmisartan and placebo groups. Aortic pulse wave velocity significantly increased with altitude (P<0.001) from 7.41±1.25 m/s at sea level to 7.70±1.13 m/s at 3400 m and to 8.52±1.59 m/s at arrival at 5400 m (P<0.0001), remaining elevated during prolonged exposure to this altitude (8.41±1.12 m/s; P<0.0001). Subendocardial oxygen supply/demand index significantly decreased with acute exposure to 3400 m: from 1.72±0.30 m/s at sea level to 1.41±0.27 m/s at 3400 m (P<0.001), remaining significantly although slightly less reduced after reaching 5400 m (1.52±0.33) and after prolonged exposure to this altitude (1.53±0.25; P<0.001). In conclusion, the acute exposure to hypobaric hypoxia induces aortic stiffening and reduction in subendocardial oxygen supply/demand index. Renin-angiotensin-aldosterone system does not seem to play any significant role in these hemodynamic changes. Clinical Trial Registration - URL: https://www.clinicaltrialsregister.eu/. Unique identifier: 2008-000540-14

    Disappearance of isocapnic buffering period during increasing work rate exercise at high altitude

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    Background At sea level, ventilation kinetics are characterized during a ramp exercise by three progressively steeper slopes, the first from the beginning of exercise to anaerobic threshold, the second from anaerobic threshold to respiratory compensation point, and the third from respiratory compensation point to peak exercise. In the second ventilation phase, body CO2 stores are used to buffer acidosis owing to lactate production; it has been suggested that this extra CO2 production drives the ventilation increase. At high altitude, ventilation increases owing to hypoxia. We hypothesize that ventilation increase reduces body CO2 stores affecting ventilation kinetics during exercise. Design In eight healthy participants, we studied the ventilation kinetics during an exercise performed at sea level and at high altitude (4559 m). Methods We used 30 W/2 min step incremental protocol both at sea level and high altitude. Tests were done on a cycloergometer with breath-by-breath ventilation and inspiratory and expiratory gas measurements. We evaluated cardiopulmonary data at anaerobic threshold, respiratory compensation point, peak exercise and the VE/VCO2 slope. Results At high altitude: (a) peak Vo(2) decreased from 2595 +/- 705 to 1745 +/- 545mi/min (P < 0.001); (b) efficiency of ventilation decreased (VE/VCO2 slope from 25 +/- 2 to 38 +/- 4, P < 0.0001); (c) at each exercise step end-tidal pressure change for CO2 was lower; and (d) the isocapnic buffering period disappeared in seven over eight participants and was significantly shortened in the remaining participant. Conclusion Exercise performed at high altitude is characterized by two, instead of three, ventilation slopes

    High-altitude hypoxia and periodic breathing during sleep: gender-related differences

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    High-altitude exposure is characterized by the appearance of periodic breathing during sleep. Only limited evidence is available, however, on the presence of gender-related differences in this breathing pattern. In 37 healthy subjects, 23 male and 14 female, we performed nocturnal cardio-respiratory monitoring in the following conditions: (1) sea level; (2) first/second night at an altitude of 3400 m; (3) first/second night at an altitude of 5400 m and after a 10 day sojourn at 5400 m. At sea level, a normal breathing pattern was observed in all subjects throughout the night. At 3400 m the apnea-hypopnea index was 40.3 ± 33.0 in males (central apneas 77.6%, central hypopneas 22.4%) and 2.4 ± 2.8 in females (central apneas 58.2%, central hypopneas 41.8%; P < 0.01). During the first recording at 5400 m, the apnea-hypopnea index was 87.5 ± 35.7 in males (central apneas 60.0%, central hypopneas 40.0%) and 41.1 ± 44.0 in females (central apneas 73.2%, central hypopneas 26.8%; P < 0.01), again with a higher frequency of central events in males as seen at lower altitude. Similar results were observed after 10 days. With increasing altitude, there was also a progressive reduction in respiratory cycle length during central apneas in males (26.9 ± 3.4 s at 3400 m and 22.6 ± 3.7 s at 5400 m). Females, who displayed a significant number of central apneas only at the highest reached altitude, were characterized by longer cycle length than males at similar altitude (30.1 ± 5.8 s at 5400 m). In conclusion, at high altitude, nocturnal periodic breathing affects males more than females. Females started to present a significant number of central sleep apneas only at the highest reached altitude. After 10 days at 5400 m gender differences in the apnea-hypopnea index similar to those observed after acute exposure were still observed, accompanied by differences in respiratory cycle length

    Changes in subendocardial viability ratio with acute high-altitude exposure and protective role of acetazolamide

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    High-altitude tourism is increasingly frequent, involving also subjects with manifest or subclinical coronary artery disease. Little is known, however, on the effects of altitude exposure on factors affecting coronary perfusion. The aim of our study was to assess myocardial oxygen supply/demand ratio in healthy subjects during acute exposure at high altitude and to evaluate the effect of acetazolamide on this parameter. Forty-four subjects (21 men, age range: 24-59 years) were randomized to double-blind acetazolamide 250 mg bid or placebo. Subendocardial viability ratio and oxygen supply/demand ratio were estimated on carotid artery by means of a validated PulsePen tonometer, at sea level, before and after treatment, and after acute and more prolonged exposure to high altitude (4559 m). On arrival at high altitude, subendocardial viability ratio was reduced in both placebo (from 1.63±0.15 to 1.18±0.17; P<0.001) and acetazolamide (from 1.68±0.25 to 1.35±0.18; P<0.001) groups. Subendocardial viability ratio returned to sea level values (1.65±0.24) after 3 days at high altitude under acetazolamide but remained lower than at sea level under placebo (1.42±0.22; P<0.005 versus baseline). At high altitude, oxygen supply/demand ratio fell both under placebo (from 29.6±4.0 to 17.3±3.0; P<0.001) and acetazolamide (from 32.1±7.0 to 22.3±4.6; P<0.001), its values remaining always higher (P<0.001) on acetazolamide. Administration of acetazolamide may, thus, antagonize the reduction in subendocardial oxygen supply triggered by exposure to hypobaric hypoxia. Further studies involving also subjects with known or subclinical coronary artery disease are needed to confirm a protective action of acetazolamide on myocardial viability under high-altitude exposure

    Effetto di beta-bloccanti selettivi e non selettivi sulla performance all’esercizio in alta quota

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    Revera M., Valentini M., Bilo G., et al. Effetto di beta-bloccanti selettivi e non selettivi sulla performance all’esercizio in alta quota. Giornal Ital Cardiol 2008. 9: 258-

    Scomparsa del tamponamento isocapnico in quota

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    Magrì D., Valenti M.C., Revera M., et al. Scomparsa del tamponamento isocapnico in quota. G Ital di Cardiol 2007. 12: 178
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