Kourounakis P, Selye H
J Pharm Sci. 1976 Dec;65(12):1838-40. doi: 10.1002/jps.2600651236.
In female rats, pretreatment with dexamethasone acetate or triamcinolone reduced the toxicity and plasma concentrations of tetraethylammonium bromide while increasing its level in urine. Pretreatment with corticosterone acetate or pregnenolone-16alpha-carbonitrile shared none of these effects. Although starvation or restraint neither diminished the tetraethylammonium bromide concentrations in plasma nor accelerated its urinary excretion, its toxicity was diminished by the stress induced with spinal cord lesions, heat, cold, hydrocortisone, or reserpine as well as starvation or restraint. The protection offered against the toxicant by stress and by the potent glucocorticoids seemed to be mediated, at least partly, via different mechanisms. Stress-induced resistance to tetraethylammonium bromide could not be attributed to elevated plasma corticosterone levels, whereas glucocorticoid-induced resistance could be partially ascribed to increased urinary excretion of the toxicant.
在雌性大鼠中,用醋酸地塞米松或曲安奈德预处理可降低溴化四乙铵的毒性和血浆浓度,同时增加其尿中水平。用醋酸皮质酮或孕烯醇酮-16α-腈预处理则无这些作用。尽管饥饿或束缚既不降低血浆中溴化四乙铵的浓度,也不加速其尿排泄,但脊髓损伤、热、冷、氢化可的松或利血平以及饥饿或束缚所诱导的应激可降低其毒性。应激和强效糖皮质激素对毒物的保护作用似乎至少部分是通过不同机制介导的。应激诱导的对溴化四乙铵的抗性不能归因于血浆皮质酮水平升高,而糖皮质激素诱导的抗性可部分归因于毒物尿排泄增加。