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大鼠在模拟4000米高原生活的低压性缺氧中,大脑皮层内β-受体密度表现为先升高,后逐渐降至正常范围。肺内β-受体密度为先降低,后升高,再恢复至正常范围。缺氧7天后回到常压中的第1天,大脑皮层和肺内β-受体密度都出现中度升高,6天内恢复正常。在整个缺氧及返回常压的过程中,Kd值变化不明显,n_H接近1。氢化可的松、地塞米松和倍他米松都可明显升高正常大鼠大脑皮层和肺内β-受体密度,而对缺氧状态下大鼠大脑皮层内β-受体影响不显著,但仍可明显增加肺内β-受体密度。提示,糖皮质激素类药物逆转缺氧初期肺内β-受体密度下降,可能对肺功能的改善具有良好作用。
In hypobaric hypoxia, which simulates the 4000-meter plateau, the β-adrenoceptor density in the cerebral cortex increased first and then gradually decreased to the normal range. Beta-receptor density in the lungs decreased first, then increased, and then returned to normal range. On the first day after returning to normal pressure after 7 days of hypoxia, the β-receptor density in the cerebral cortex and lung increased moderately and returned to normal within 6 days. In the whole process of hypoxia and return to normal pressure, the Kd value did not change significantly, n_H close to 1. Hydrocortisone, dexamethasone and betamethasone can significantly increase the normal rat cerebral cortex and lung β-receptor density, and hypoxia in the rat cortex β-receptor had no significant effect, But still can significantly increase the lung β-receptor density. Tip, glucocorticoid drugs to reverse the early hypoxia lung β-receptor density decreased, may improve pulmonary function has a good effect.