Project/Area Number |
07457146
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
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Research Institution | SHINSHU UNIVERSITY SCHOOL OF MEDICINE |
Principal Investigator |
KOBAYASHI Toshio SHINSHU UNIVERSITY SCHOOL OF MEDICINE,ASSISTANT PROFESSOR, 医学部・附属病院, 講師 (80020775)
|
Co-Investigator(Kenkyū-buntansha) |
YOSHIMURA Kazuhuko SHINSHU UNIVERSITY SCHOOL OF MEDICINE,ASSOCIATE PROFESSOR, 医学部・加齢適応センター, 助教授 (70174985)
MATSUZAWA Yukinori SHINSHU UNIVERSITY SCHOOL OF MEDICINE,ASSISTANT PROFESSOR, 医学部・附属病院, 助手 (40219423)
KUBO Keishi SHINSHU UNIVERSITY SCHOOL OF MEDICINE,ASSISTANT PROFESSOR, 医学部, 講師 (80143965)
斉藤 覚 信州大学, 医学部・附属病院, 講師 (20175350)
藤本 圭作 信州大学, 医学部・附属病院, 助手 (70242691)
|
Project Period (FY) |
1995 – 1996
|
Project Status |
Completed (Fiscal Year 1996)
|
Budget Amount *help |
¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 1996: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1995: ¥5,300,000 (Direct Cost: ¥5,300,000)
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Keywords | maximal oxygen uptake / anaerobic threhold / oxygen transport / high altitude / pulmonary edema / acute mountain sicknes / endothelin / HLA / 最大換気量 / 低酸素 / 肺血流シンチグラム / 肺血管収縮反応 / 低酸素性肺血管収縮反応 / 低酸素換気抑制 / 酸素摂取量 / 高地適応 |
Research Abstract |
1) EFFECTS OF EXERCISE AT HIGH ALTITUDE ON CARDIOPULMONARY FUNCTION a) To examine the difference for oxygen transport between Tibetan living for generations at high altitude a acclimatized Han newcomers to high altitude, we measured the ventilatory, circulatory, metabolic and gas exchanges function during exercise in 17 Tibetans and 19 Hans at the altitude of 3417m in China. At maximal effort, the Tibetans, compared with the Hans, showed higher O2 consumption, stroke volume, cardiac output, and the maximal ventilation. The anaerobic threshold for absolute O2 consumption for the Tibetan are highent for the Hans. We conclude that the lifelong exposure to an hypoxic environment has resulted in an increase in oxygen transport and improved aerobic exercise performance. b) The difference of oxygen transport between adolescents of lifelong Tibetans and acclimatized Han newcomers to high altitude was studied. We found that the exposure to high altitude from birth to adolescence resulted in an ef
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ficient oxygen transport and a greater aerobic exercise performance which may reflect a successful adaptation to life at high altitude. 2) PATHOPHYSIOLOGY OF HIGH ALTITUDE PULMONARY EDEMA a) We have previously shown that high altitude pulmonary edema-susceptible subjects (HAPE-S) have an accentuated pulmonary vascular response to hypoxia. We investigated the relationship between plasma endothelin-1 levels and the acute hypoxic pulmonary vascular response in patients with HAPE-S and healthy control subjects. We found that the increased pulmonary vascular response to acute hypoxia in HAPE-S may n related to endothelin-1 release. b) The cytokines were measured in the bronchoalveolar lavage fluid from four patients with HAPE.The leves IL-1*IL-6, II-8, and TNFalpha were considerably increased but returned quickly to the normal ranges or wel not detected after recovery. The levels of IL-1alpha, IL-10, and P-selectinlevels didi not change. These rest suggest that an inflammatory process almost identical with ARDS may occur in HAPE,but that these changes transient. c) We examined the pulmonary hemodynamic response to hypoxia in HAPE susceptible subjects by radioisotop scintigraphy. We performed ventilation-perfusion scintigraphyand acquired functional images of Q V and V/Q the functional images, the pulmonary blood flow was significantly shifted from the lower lung field to the upp lung field under hypoxia but no significant change of regional ventilation was observed in the HAPE-susceptibl subjects. As a results, they showed ventilation-perfusion mismatch. d) We studied whether human leukocyte antigen DR-6 functions as agenetic predisposition to HAPE.The frequency of DR-6 was increased in the subjects susceptible to HAPE,which suggests that they have a constitutional abnormality in the pulmonary circulatory, and ventilatory responses to hypoxia and hyhobaria, and that genetic factors may be involved in the development of HAPE. Less
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