Derivatives of p-aminobenzoic acid and their action on the growth of bacteria
SummaryVarious derivatives of P.A.B. obtained by introduction of substituents in the benzene-nucleus have been examined for their action on the growth ofAerobacter aerogenes in a simple synthetic medium and ofDiplococcus pneumoniae in ascites-broth without peptone.The following results have been obtained:1.The 2-amino, 3-amino, 3-chloro, 3-bromo, 2-methyl, 3-methyl, and 2.3-dimethyl derivatives of P.A.B., and also 2-sulfanilamido-4-aminobenzoic acid have sulfonamide activity.2.The 2-hydroxy, 2-fluoro, and 2-nitro derivatives have an antisulfonamide activity similar to the activity of P.A.B., although weaker.3.The 3-hydroxy, 2-chloro, and 2-bromo derivatives show sulfonamide-activity in relatively high concentrations. In lower concentrations they act as anti-sulfonamides.4.The 3-nitro, 2.6-dimethyl, and 3.5-dimethyl derivatives, and methyl 2-acetamino-4-amino-benzoate are completely inactive. These results have been compared with those of other investigators and the causes of some contradictions have been elucidated.
Dérivés simples de l'acide p-aminobenzoïque agissant comme sulfonamides et antisulfonamides
RésuméPour plusieurs dérivés de l'acide p-aminobenzoïque, substitués dans le noyau, on a examiné l'activité sulfonamide ou anti-sulfonamide sur des pneumocoques “in vitro”.Les acides 2,4-diamino- et 3,4-diamino-benzoïques exercent la même action bactériostatique que la sulfanilamide. Les acides 2-chloro- et 2-bromo-4-aminobenzoïques empêchent l'action inhibitrice de la sulfanilamide. Quelques autres dérivés ne présentent nulle activité.
Electrophysiological Studies of Penticainide (CM 7857), a New Antiarrhythmic Agent, in Mammalian Myocardium
The intracellular electrophysiologic properties of a new antiarrhythmic substance, penticainide, were studied in isolated rabbit, dog, and guinea pig myocardial preparations superfused or perfused with oxygenated Tyrode's solution. “Therapeutic” concentrations of penticainide (1.5 to 3 x 10-5 M) had little effect on sinus node automaticity; sinoatrial conduction was slightly delayed. In atrial, Purkinje and ventricular fibers, amplitude, and maximal rate of rise of phase 0 (dV/dtmax) were decreased by penticainide; Purkinje-ventricle conduction velocity was depressed. Penticainide did not significantly modify action potential duration (APD) of rabbit atria and dog ventricle and reduced APD and effective refractory period (ERP) of dog Purkinje and guinea pig ventricular fibers. Penticainide reduced APD heterogeneity of Purkinje-ventricle junction with a preferential effect at the gate and decreased tension amplitude of perfused papillary muscle in dog heart. The effect of penticainide on dV/dtmax was voltage and rate dependent; the resting block was weak. Thus, penticainide is a class 1 antiarrhythmic agent with properties of class 1B agents such as APD reduction and properties of class 1C agents such as slow recovery kinetic of rate-dependent block.