| Co-Investigator(Kenkyū-buntansha) |
SAKAI Akio SHINSHU UNIV., SCH.OF MED., ASSOCIATE PROFESSOR, 医学部・附属心脈管病研究施設, 助教授 (70020758)
KUBO Keishi SHINSHU UNIV., SCH.OF MED., ASSISTANT PROFESSOR, 医学部, 講師 (80143965)
KOBAYASHI Toshio SHINSHU UNIV., SCH.OF MED., ASSISTANT PROFESSOR, 医学部, 講師 (80020775)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1993: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1992: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Research Abstract |
In this project three studies were performed. First study was to investigate the role of nocturnal periodic breathing (PB) and sleep-induced oxygen desaturation in the pathophysiology of acute mountain sickness (AMS). Nine healthy male lowlanders, including three subjects with at least one history of HAPE (HAPE-S), were exposed to a simulated altitude of 3,700m for 24h in a hypobaric cham ber. Twelve hours after arriving, sleep study was started. All subjects showed lower Sa02 during sleep than awake, and symptoms of AMS were more intense the next morning. The sleep desaturation tended to be more intense in subjects with higher AMS-score and with lower sea level hypoxic ventilatory response (HVR). The time spent in PB, however, was not correlated significantly with the degree of sleep desaturation, the severity of AMS, or HVR.Second, the effect of hypoxic ventilatory depression (HVD) in HAPE was examined. In the study of exposure to 3,200 m, one of HAPE-susceptible subjects (HAPE-S), who exhibited the lowest Pa02 at the altitude, had a paradoxical increase in ventilation by 100% oxygen breathing. In the same subject, sleep-related abnormal irregular breathing disappeared completely after supplemrntal oxygen in the above-mentioned 3,700m-study. Third, ventilatory response to exercise at sea level in HAPE-S was examined at low altitude. Mild exercise (25-50 watt) developed an excessive pulmonary hypertension with severe hypoxemia in HAPE-S.Changes in pH and PaC02, however, were not significantly defferent between HAPE-S and control subjects. These three studies suggest that relative alveolar hypoventilation, HVD, sleep desaturation, which may be due to low HVR, may contribute to the development or worsening of AMS, and may lead to HAPE in severe cases. Nocturnal PB and lower ventilatory response to exercise at high altitude, however, could not be determined as contributing factors in the pathogenesis of AMS or HAPE in this project.
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