Saligaut C, Moore N, Boulu R, Plotkine M, Leclerc J L, Prioux-Guyonneau M, Boismare F
Aviat Space Environ Med. 1981 Mar;52(3):166-70.
The learning of a conditioned avoidance response, the catecholamine levels in some cerebral structures, and the evolution of the cortical PO2, were studied under hypobaric hypoxia (300 torr) and under normoxia, in rats treated or not with apomorphine, at the dose of 1 or 10 mg/kg i.p. Apomorphine at 1 mg/kg improves the learning capacity and stabilises the cerebral catecholamine levels under hypoxia; no modification of the evolution of the cortical PO2 during hypoxia was observed between control rats and rats treated with this dose of apomorphine. Apomorphine at 10 mg/kg totally inhibits learning under normoxia or hypoxia. It is therefore possible to suppose that the antihypoxic protective mechanism of low-dose apomorphine is due to a stabilization of the levels of both dopamine and noradrenaline during hypoxia, but not to an increase in the cerebral oxygen availability. These data suggest the clinical possibility of using other dopaminergic stimulating agents for their eventual antihypoxic properties.
在低压缺氧(300托)和常氧条件下,对腹腔注射1或10毫克/千克阿扑吗啡或未注射阿扑吗啡的大鼠,研究了条件性回避反应的学习、某些脑结构中的儿茶酚胺水平以及皮质PO2的变化。1毫克/千克的阿扑吗啡可提高缺氧条件下的学习能力并稳定脑内儿茶酚胺水平;在对照大鼠和用该剂量阿扑吗啡处理的大鼠之间,未观察到缺氧期间皮质PO2变化的改变。10毫克/千克的阿扑吗啡在常氧或缺氧条件下完全抑制学习。因此,可以推测低剂量阿扑吗啡的抗缺氧保护机制是由于缺氧期间多巴胺和去甲肾上腺素水平的稳定,而不是由于脑氧供应的增加。这些数据提示了使用其他多巴胺能刺激剂发挥其潜在抗缺氧特性的临床可能性。