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目的:研究β-内啡肽对急性低氧暴露下清醒大鼠下丘脑正中隆起和室旁核促甲状腺素释放激素(TRH)应答的影响.方法:放射免疫法测定脑组织TRH和血清T_3、T_4含量.雄性大鼠放置于低压舱中,模拟海拔7000米(8.2％ O_2),低氧暴露时间2 h.低氧暴露前,侧脑室注射β-内啡肽.结果:侧脑室分别注射β-内啡肽0.l和1μmol/L使低氧暴露大鼠下丘脑正中隆起TRH含量分别比生理盐水组[(4.8±0.3)μg/g蛋白]升高12％(P<0.05)和15％(P<0.0 5),室旁核TRH含量分别比生理盐水组[(180±21)ng/g蛋白]升高24％(P<0.05)和44％(P<0.01),血清 T_3、T_4浓度降低(P<0.05或P<0.01).纳洛酮10 μmol/L拮抗了 β-内啡肽0.1μmol/L对室旁核和正中隆起TRH含量升高以及血清T_3、T_4降低的效应.单独脑室注射纳洛酮10 μmol/L使下丘脑正中隆起和室旁核TRH减少(P<0.05或P<0.01),而血清T_3、T_4浓度升高(P<0.01).结论:β-内啡肽通过抑制正中隆起和室旁核TRH释放机制参与急性低氧暴露大鼠下丘脑TRH分泌的调节.
AIM: To investigate the effect of β-endorphin on the hypothalamic upregulation of hypothalamus and thyroid-stimulating hormone (TRH) response in paraventricular nucleus in acute hypoxic exposure.Methods: Radioimmunoassay was used to detect the levels of TRH and T_3 and T_4 in serum Content.Male rats were placed in the low-pressure cabin, the simulated altitude of 7000 meters (8.2% O_2), hypoxia exposure time 2 h before hypoxia exposure, intracerebroventricular injection of β-endorphin.Results: Intracerebroventricular injection of β- Endorphins 0.1 and 1 μmol / L increased the content of TRH in the hypothalamus midgut elevated 12% (P <0.05) and 15% (P <0.05), respectively, compared with saline group (P <0.05). The levels of TRH in paraventricular nucleus were increased by 24% (P <0.05) and 44% (P <0.01) respectively compared with [180 ± 21] ng / g protein in normal saline group (P <0.05 or P <0.01), naloxone 10 μmol / L antagonized the effect of 0.1 μmol / L β-endorphin on the increase of TRH and the decrease of serum T 3 and T 4 in paraventricular nucleus and median eminence. The intracerebroventricular injection of naloxone 10 μmol / L reduced TRH in the hypothalamus and paraventricular nucleus (P <0.05 or P <0.01), while serum T 3 and T 4 concentrations increased (P <0.01) .Conclusion: β-endorphin Peptides inhibit the median bulge and paraventricular nucleus TRH Release Mechanism Involved in Regulation of TRH Secretion in Hypothalamus of Rats with Acute Hypoxic Exposure.