Saligaut C, Moore N, Chretien P, Daoust M, Richard O, Boismare F
Stroke. 1982 Nov-Dec;13(6):859-64. doi: 10.1161/01.str.13.6.859.
Previous data have established that postsynaptic stimulation of central dopaminergic receptors was mainly involved in the protective action of apomorphine against the comportmental consequences of hypobaric hypoxia in rats: disturbances in a conditioned avoidance response. We confirm this notion showing that domperidone (a peripheral dopaminergic blocking agent) does not antagonize the protective effect of apomorphine. Furthermore, we establish that the action of apomorphine is at least partially mediated by adrenal glands since it is no longer seen in adrenalectomized rats. In normal rats, apomorphine enhances the corticosterone increase which is observed during hypobaric hypoxia and decreases the hypoxia-induced elevation of the adrenaline level. It is therefore concluded that the anti-hypoxic activity of apomorphine is probably mediated by a centrally mediated dopaminergic modification of the adrenal response to hypobaric hypoxia.
先前的数据表明,中枢多巴胺能受体的突触后刺激主要参与了阿扑吗啡对大鼠低压缺氧行为后果(条件性回避反应障碍)的保护作用。我们通过实验证实了这一观点,即多潘立酮(一种外周多巴胺能阻断剂)不会拮抗阿扑吗啡的保护作用。此外,我们还发现阿扑吗啡的作用至少部分是由肾上腺介导的,因为在肾上腺切除的大鼠中不再观察到这种作用。在正常大鼠中,阿扑吗啡会增强低压缺氧期间观察到的皮质酮增加,并降低缺氧诱导的肾上腺素水平升高。因此得出结论,阿扑吗啡的抗缺氧活性可能是由中枢介导的多巴胺能对肾上腺对低压缺氧反应的调节所介导的。