| Co-Investigator(Kenkyū-buntansha) |
SAKAI Akio Shinshu University School of Medicine Department of Environmental Physiology Ass, 医学部・附属心脈管研究施設, 助教授 (70020758)
KUBO Keishi Shinshu University School of Medicine First Department of Internal Medicine Assi, 医学部, 講師 (80143965)
HANDA Kenjiro Shinshu University School of Medicine First Department of Internal Medicine Asso, 医学部, 助教授 (70020724)
平山 二郎 信州大学, 医学部附属病院, 助手 (90156696)
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| Budget Amount *help |
¥8,500,000 (Direct Cost: ¥8,500,000)
Fiscal Year 1990: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1989: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Research Abstract |
(1) Blunted hypoxic ventilatory drive in subjects susceptible to high-altitude pulmonary edema
Some previous studies suggest the relationship between the blunted hypoxic ventilatory responses (HVR) and high-altitude pulmonary edema (HAPE). To examine whether all the HAPE-susceptible subjects consistently show blunted HVR at low altitude, we evaluated the conventional pulmonary function test, HVR and hypercapnic ventilatory responese (HCVR) in ten lowlanders who had a previous history of HAPE and compared these results with those of eight control lowlanders who had no history of HAPE. HVR was measured by the progressive isocapnic hypoxic method and was evaluated by the slope relating minute ventilation to arterial O2 saturation. HVCR was measured by the rebreathing method of Read. In HVCR, HAPE-susceptible subjects showed relatively lower S-value, but there was no significant difference between the two group. On the other hand, HAPE-susceptible subjects showed significantly lower HVR tha
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n control subjects. These results suggest that HAPE-susceptible subjects more frequently show low HVR at low altitude. It would seem therefore that low HVR alone need not be a critical factor for HAPE. This could be one of several contribruting factors.
(2) Hemodynamic responses to acute hypoxia, hypobaria, and exercise in subjects susceptible to high-altitude pulmonary edema.
To clarify the presence of the constitutional abnormality implicated in the pathogenesis of high-altitude pulmonary edema, we evaluated the hemodynamic responses to hypoxia, hypobaria, and exercise in HAPE-susceptible subjects (HAPE-S). HAPE-S were five males with a history of HAPE. Five healthy volunteers who had repeated experiences of mountain climbing without any history of altitude-related problems served as controls. HAPE-S showed much greater increase in pulmonary vascular resistance index (PVRI) than the controls subjects, resulting in a much higher level of pulmonary arterial pressur (Ppa), under both acute hypoxia 15%, and acute hypobaria of 515 Torr. Also PVRI in HAPE-S exhibited a tendency to increase even during light exercise with supine bicycle ergometer, whereas PVRI in HAPE-S in the control subjects significantly decreased, so that HAPE-S showed a greater increase in Ppa and a greater decrease in arterial oxygen tension. We thus conclude that HAPE-S have a constitutional abnormality, which can be evaluated at low altitude, in the pulmonary circulatory responses to possible causative factors of HAPE such as hypoxia, hypobaria, and exercise.
(3) Doppler assessment of pulmonary hypertension induced by hypoxic breathing in subjects susceptible to high altitude pulmonary edema.
We examined the hemodynamic responses to hypoxia in HAPE susceptible subjects (HAPE-S) by means of both right heart catheterization and pulsed Doppler echocardiography. The HAPE-S were seven men and one woman with a history of HAPE. Six healthy volunteers who had repeated experiences of mountain climbing without any history of altitude-related problems served as control subjects. The HAPE-S showed much greater increase in pulmonary vascular resistance (PVR) than the control subjects, resulting in a much higher level of pulmonary arterial pressure (Ppa) under acute hypoxia both of 15% O2 and 10% O2. We then evaluated the usefulness of pulsed Doppler echocardiography in the prediction of pulmonary hypertension. Acceleration time (AcT) and right ventricular ejection time (RVET) were measured from the flow velocity pattern in the right ventricular outflow tract. The ratio of AcT to RVET were measured was correlated to invasively determined mean Ppa and PVR. We conclude that pulsed Doppler echocardiography may be supportive to assess the pulmonary vascular pressor response in the HAPE-S. Less
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