Bounous H, Cagin N, Levitt B, Somberg J
Br J Pharmacol. 1978 May;63(1):73-7. doi: 10.1111/j.1476-5381.1978.tb07776.x.
The capacity of diphenidol to influence ouabain-induced cardiotoxicity was studied in anaesthetized cats with and without spinal cord transection. 2 Diphenidol pretreatment increased the lethal dose of ouabain in both intact cats and cats in which the spinal cords had been transected. Diphenidol pretreatment increased the myocardial content of ouabain associated with death in the intact animals, but failed to influence the lethal ventricular concentration in cats with transected spinal cords. 3 The failure of diphenidol to influence tissue thresholds for toxicity in the spinal cat and the equivalence of tissue ouabain requirements for death in spinal cats and diphenidol-treated intact animals, suggest a neural mechanism for the protective effect in intact animals. 4 Ouabain administration prolonged atrio-ventricular conduction time in all animals and diphenidol attenuated this effect. Thus, the influence of both drugs on antrioventricular conduction may not be entirely mediated by central neurones.
在麻醉猫身上,研究了地芬尼多对哇巴因诱导的心脏毒性的影响,实验对象包括脊髓完整和脊髓横断的猫。2地芬尼多预处理增加了完整猫和脊髓横断猫的哇巴因致死剂量。地芬尼多预处理增加了完整动物死亡时心肌中的哇巴因含量,但未能影响脊髓横断猫的致死性心室浓度。3地芬尼多未能影响脊髓猫的组织毒性阈值,且脊髓猫和地芬尼多处理的完整动物死亡时组织中哇巴因的需求量相当,这表明完整动物中存在一种神经机制发挥保护作用。4给予哇巴因会延长所有动物的房室传导时间,而地芬尼多可减弱这种作用。因此,两种药物对房室传导的影响可能并非完全由中枢神经元介导。