Effects of lithium chloride, desmethylimipramine and cocaine on the cardiovascular actions of ouabain in dogs with or without carotid and aortic baro-receptor reflexes.

The cardiovascular effects of ouabain as modified by LiCl, DMI and cocaine in anesthetized dogs with or without buffer nerves (carotid sinus and vagus nerves) were compared. Ouabain significantly increased the LV dp/dt in saline and cocaine but not in LiCl or DMI treated buffered animals. Significant ouabain-induced increase in MAP and decrease in HR were also observed in animals receiving DMI and cocaine. Neither the AD nor the LD of ouabain was modified by Licl or cocaine. DMI, while reducing the AD could not modify the LD of ouabain. In animals without the baro-reflex mechanism (debuffered), significant increase in both LVP and LV dp/dt were observed with ouabain following LiCl and DMI administration. Debuffering itself reduced the LD ouabain in saline treated animals. It was concluded that depending on the presence or absence of baro-reflex mechanism, lithium and DMI could either inhibit or facilitate the inotropic effect of ouabain. Cocaine did not interfere with the actions of ouabain. Ouabain-induced cardiotoxicites were not greatly modified by any of the drugs used.