| Co-Investigator(Kenkyū-buntansha) |
SAKAI Akio Shinshu Univ., Sch. of Med., Associate Professor, 医学部附属心脈管研究施設, 助教授 (70020758)
UEDA Gou Shinshu Univ., Sch. of Med., Professor, 医学部附属心脈管研究施設, 教授 (10020702)
SEKIGUCHI Morie Shinshu Univ., Sch. of Med., Professor, 医学部, 教授 (70075232)
KUBO Keishi Shinshu Univ., Sch. of Med., Assistant Professor, 医学部, 講師 (80143965)
KOBAYASHI Toshio Shinshu Univ., Sch. of Med., Assistant Professor, 医学部附属病院, 講師 (80020775)
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| Research Abstract |
In this project we have performed the two main studies. First study was to investigate the role of hypoxic ventilatory response (HVR) in the pathogenesis of acute mountain sickness (AMS). Nine healthy male lowlanders were exposed to a simulated altitude of 3, 700m for 24h in a hypobaric chamber. Those subjects with lower alveolar ventilation on arrival at 3, 700m subsequently developed more severe AMS 24h after the exposure. They also showed lower HVR at low altitude. These results suggest that low HVR contributes to the development of AMS. We have also examined impaired pulmonary gas exchange, cerebral edema, and sleep apnea in the pathogenesis of AMS.
Secondly we investigated the role of low HVR in the pathophysiology of high-altitude pulmonary edema (HAPE). Nine subjects with a history of HAPE (HAPE-S) and six control subjects were exposed to a simulated altitude of 3, 200m. At low altitude HVR in HAPE-S was significantly lower than that of controls. At high-altitude HAPE-S showed lesser increase in V_E, lower P_A, lower PaO2 and higher PaCO2 compared with control subjects. In one of the HAPE-S, who showed the lowest PaO2 at the simulated altitude, 100% oxygen breathing developed a paradoxical increase in ventilation, suggesting hypoxic ventilatory depression (HVD). These results suggest that relative hypoveritilation, which may be due to low HVR and/or HVD, may contribute to the exaggerated hypoxemia occurred during exposure to high altitude in HAPE-S.
These two studies suggest that low HVR could be one of the contributing factors in AMS and even in HAPE. However, the exact mechanism which may lead to pulmonary edema remains unclear. Moreover, not all HAPE-S showed low HVR. We need further studies on abnormal control of ventilation in HAPE or AMS, such as respiratory control in exercise and sleep at altitude, relationship between cerebral edema and HAPE, and the role of HVD in HAPE.
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