低压性缺氧及糖度质激素类药物对大鼠大脑皮层和肺内β-受体的影响

Effect of hypobaric hypoxia and glucocorticoids on β-adrenoceptor in rat cerebral cortex and lung

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。

This study showed that when the rat lived in simulated altitude of 4000 m. the β-receptor number in cerebral cortex increased first, then returned to normal gradually. The receptor number in rat lung reduced first. then rose high above the normal, and then dropped to normal. On the first day after the rats returned to normal atmosphere the β-receptor number in both tissues increased moderately. No significant change of Kd values was observed in the experimental groups. The Hill numbers were around 1. The hydrocortisone, dexamethasone and betamethasone could increase β-receptor number in both tissues of normal rats, and had the same effect on hypoxic rat cerebral cortex. The results mentioned above indicate that the three glucocorticoids can reverse the reduction of β-receptor number in rat lung during the initial stage of hypoxla, which may lead part of the beneficial effect of glucocorticoids on high-altitude disease.