| Project/Area Number |
63480116
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
環境生理学(含体力医学･栄養生理学)
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| Research Institution | Nagoya University |
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Principal Investigator |
MATSUI Nobuo Nagoya Univ. the Res. Inst. of Environ, Med, Prof., 環境医学研究所, 教授 (50023643)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAMOTO Norihiro Nagoya Univ. the Res. Inst. of Environ. Med, Assist. Prof., 環境医学研究所, 助手 (10221615)
MURATA Yoshiharu Nagoya Unev. the Res. Inst. of Environ Med, Assist. Prof., 環境医学研究所, 助手 (80174308)
SEO Hisao Nagoya Univ. the Res. Inst. of Environ. Med, Assoc. Prof., 環境医学研究所, 助教授 (40135380)
井上 達 名古屋大学, 環境医学研究所, 助手 (80184737)
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| Project Period (FY) |
1988 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 1990: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1988: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Acute mountain sickness / Water and electrolyte metabolism / Alkalosis / Anti-diuretic hormone / Aldosterone / Cortisol / Parathyroid hormone / Dexamethasone / カルシウム代謝 / 燐代謝 / 腎性 cyclic AMP / 低圧・低酸素 / 登山家適性判定 / デキサメサゾン抑制 / 高地順応 / ホルモン / カルシウム・燐代謝 |
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| Research Abstract |
We previously demonstrated that the change in water-electrolyte metabolism, which is thought to be one of the major precipitating factors of acute mountain sickness, is exacerbated by increased secretion of water-electrolyte-regulating hormones and that simulated high altitude exposure causes a rise of serum calcium and a fall of serum phosphate. Thus, present study is aimed to investigate (1) the influence of the suppression of secretion or an inhibition of action of water-electrolyte-regulating hormones on the water and electrolyte metabolism under simulated altitude exposure, (2) a possibility to evaluate the susceptibility to acute mountain sickness by comparing suppressibility of hormone responses to altitude exposure between climbers and non-climbers, (3) whether parathyroid hormone involves in the alteration of calcium-phosphate metabolism under altitude exposure.
(1) The administration of dexamethasone attenuated water retention, alkalosis and symptomes related to acute mountain
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sickness which was induced by simulated 6,000m altitude exposure by inhibiting the rises of ADH and aldosterone. The administration of spironolactone, which blocks aldosterone action at the level of renal tubule, also attenuated the water retention and alkalosis induced by the exposure. Thus, our postulation that water-electrolyte-regulating hormones exacerbates acute mountain sickness was confirmed and the results can contribute for prevention and treatment of acute mountain sickness.
(2) The response of serum cortisol to altitude exposure can be more easily suppressed in climbers than in non-climbers. The suppressibility of cortisol well correlated with those of aldosterone and of ADH. Therefore, it may be speculated that the dexamethasone suppression test differentiates susceptibe from non-susceptible subjects to acute mountain sickness and that the test is useful to evaluate the fitness of mountain climbing.
(3) Parathyroid hormone level significantly rose during simulated altitude exposure. Nephrogenous cyclic AMP increased 2 fold by the exposure indicating increased PTH action. Urinary Ca decreased when serum Ca rose. This change is compatible with elevated PTH. On the other hand, urinary P decreased with a marked fall of serum P. This fall of serum P may be induced by increased anaerobic energy production under hypoxia. Thus, increased secretion of PTH again enhances alteration of Ca and P metabolism. The involvement of this metabolic derangement in acute mountain sickness needs further investigation. Less
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