| Project/Area Number |
61480195
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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 |
Respiratory organ internal medicine
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| Research Institution | Tottori University School of Medicine |
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Principal Investigator |
SASAKI Takao Tottori Univ. School of Medicine Professor, 医学部, 教授 (10004631)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUMOTO Yukio Tottori Univ. School of Medicine Assistant Professor, 医学部附属病院, 講師 (90135880)
HIKITA Toru Tottori Univ. School of Medicine Assistant Professor, 医学部, 講師 (70093622)
ISHITOBI Kazuyuki Tottori Univ. School of Medicine Associate Professor, 医学部, 助教授 (20032336)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | thyroid hormone / bronchial asthma / sensitized guinea pig / serum cortisol / aminophylline / 日内リズム / 気管支筋収縮 / 呼吸機能 |
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| Research Abstract |
To investigate the effects of thyroid hormone on the abnormal breathing, (1);contractility of guinea pig tracheal rings in hyperthyroid state, (2);serum cortisol after methacholine inhalation challenge, and (3);serum TSH and thyroid hormones after intravenous aminophylline administration to asthmatic patients, were measured. In hyperthyroid state, contraction of sensitized guinea pig tracheal rings to antigen was qugmented, but contraction to histamine and acetylcholoine of non-sensitized guinea pigs was inhibited. There were several patients whose serum free cortisol did not increase after methacholine inhalation challenge, and their asthmatic attacks were usually prolonged and severe. Transient intravenous aminophylline administration increased serum TSH and T_4, but serum theophylline concentrations after long term oral administration were only related to reverse T_3.
These findings suggested that thyroid hormones, T_4 and T_3, may augment the abnormal breathing in allergic asthma, and their effect may increase in the case of no adrenocortical response to asthmatic attacks because TSH release by TRH may not be suppressed by cortisol.
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