Harriet M. Maling

Ventricular Arrhythmias Induced by Sympathomimetic Amines in Unanesthetized Dogs Following Coronary Artery Occlusion

Epinephrine and norepinephrine, in doses which cause little ectopic activity in unanesthetized normal dogs, produce exaggerated ectopic responses about the fourth day after coronary ligation, when the arrhythmias caused by the ligation per se have subsided. These responses persist for approximately 12 days after ligation and suggest reactivation of latent ectopic foci. Observations with methoxamine, isoproterenol, and atropine indicate that ventricular tachycardia is easily induced after occlusion by drugs which simultaneously stimulate the myocardium and slow the sinus node rate.

Evaluation of the Effects of Cephaloridine on Urate Excretion in the Rat

In female Sprague-Dawley rats, the renal clearance of cephaloridine decreased as the plasma concentration of the drug declined from above 10 micrograms/ml to below about 3 micrograms/ml, thus suggesting a saturable tubular reabsorption of cephaloridine similar to that shown previously in man. The effects of cephaloridine (250 mg/kg i.v.) were compared with those shown by a group of rats receiving saline and another group of rats receiving probenecid (250 mg/kg i.v.). Probenecid caused a sustained increase in the urate excretion rate. By contrast, cephaloridine produced a relatively small and transient increase in urate excretion, which may have been caused by its diuretic effect. Thus, it is unlikely that the reabsorption mechanism of urate is the principle mechanism by which cephaloridine is reabsorbed.