医化学シンポジウム
Online ISSN : 2187-4069
Print ISSN : 0386-3387
ISSN-L : 0386-3387
1. 寒冷及び熱気暴露における血中ホルモンの変動
松岡 徹熊原 雄一宮井 潔岡田 義昭
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ジャーナル フリー

1971 年 10 巻 p. 85-89

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Effects of exposure to cold and hot air on hormone levels in blood, especially on growth hormone (GH), were studied in normal adult subjects.
Two male and four female subjects were exposed to cold (4°) for 1 or 2 hours in thin underclothes after overnight fasting and sitting at least for 2 hours under room temperature. Blood samples were withdrawn at an interval of 30 minutes. In the first experiment, 1 hour exposure to cold was undertaken in two male subjects. Serum GH levels showed no change nor decrease during cooling. They increased, however, from an undetectable value to 5.2mμg/ml in 30 minutes and from 2. 5 to 5.6mμg/ml in 60 minutes after cooling, respectively. Two male and four female subjects were exposed to cold for 2 hours in the second experiment. Serum GH levels did not rise during cooling but increased significantly in all the cases after rewarming under room temperature. Blood glucose and serum insulin levels did not change and NEFA increased to 113-267% of the initial values during or after cooling. Serum cortisol increased from 18.4 to 23.8μg/dl during cooling in one subject but changed little in the others.
Exposure to hot air (46-48°) for 1 hour was studied in five adult male subjects after overnight fasting. Body temperature elevated from 36.3-36.7 to 37.5-37.9° and pulse rate increased from 68-74 to 96-102/minutes in 60 minutes after exposure to hot air. Sweating was very intense and body weight decreased by 0.5 to 1.5 kg, but blood hematocrit values did not change significantly. Serum GH levels increased from 0.8-2.0 (mean 1.4) to 3.5-30 (mean 12.3) mμg/ml in 60 minutes after heating and decreased to the initial value in 60 minutes under room temperature. There was no significant change in the levels of blood glucose and serum insulin. NEFA increased to 149.5-187.6% of the initial value during or after exposure to hot air in four subjects, but the increment was little in one of the cases. Serum cortisol values did not rise significantly and serum thyroxine levels showed no change during and after exposure to hot air. Two subjects, whose serum GH increased during exposure to hot air, was administered 50 g glucose p.o. 30 minutes prior to and just before entering into the hot room and then exposed to hot air. Serum GH levels decreased from 1.0 and 1.7 to an undetectable value and 0.5 mμg/ml in 60 minutes after exposure hot air.
Serum GH levels during hypothermic surgery had been reported not to rise during the operation. However, GH secretion in this kind of operation under hypothermia might be affected by premedication with a central nervous depressant such as chlorpromazine. The present experiment of exposure to cold in normal adult subjects clarify that the exposure did not stimulate GH secretion. From the fact that serum GH levels did not rise in response to 1 or 2 hour exposure to cold and increased after rewarming, the presence of a refractory period to stimulate GH release may be denied.
The mechanism of GH release in response to exposure to hot air was not clarified. However, from the result that glucose administration completely suppresses the GH release during heating, exposure to hot air can give rise to no stress to stimulate the GH release.

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