Detail of "51-06-9"

Reference

The effect of antiarrhythmic drugs on triggered sustained rhythmic activity in cardiac Purkinje fibers

The effect of antiarrhythmic drugs on triggered sustained rhythmic activity in cardiac Purkinje fibers. Arnsdorf, Morton F.; Sawicki, George J. (Pritzker Sch. Med., Univ. Chicago, Chicago, Ill., USA). J. Pharmacol. Exp. Ther., 201(3), 689-700 (English) 1977. CODEN: JPETAB. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Triggered sustained rhythmic activity (TSRA) was seen in eight sheep Purkinje fibers during the course of microelectrode studies. This TSRA had the following characteristics: (1) it was obsd. in Purkinje fibers having otherwise essentially normal membrane properties; (2) it occurred when the Purkinje fibers were bathed in physiologic Tyrode's solution at [K]0 = 4 mM; (3) a single electrically induced action potential initiated either sustained nondriven action potentials or oscillations that increased in amplitude eventuating in sustained nondriven action potentials; and (4) either it terminated spontaneously by reaching repolarization threshold with a return to the resting transmembrane voltage (Vr) or persisted essentially indefinitely until terminated by intracellularly applied hyperpolarizing current. Procaine amide [51-06-9], lidocaine (I) [137-58-6] and a .beta.-receptor blocker tolamolol [38103-61-6] were effective against TSRA. Current-voltage relationships were performed using two microelectrodes: one for intracellular current application; the other for transmembrane voltage recording. Procaine amide decreased the amplitude of nondriven sustained action potentials and, in time, often resulted in one or two steady quiescent states: at about -30 mV and/or Vr. I did not decrease the nondriven sustained action potential amplitude, but made its maximal diastolic transmembrane voltage more negative thereby permitting attainment of the repolarization threshold and a return to Vr: am action suggested by the current-voltage relationships to be mediated by increasing membrane potassium conductance. The effects of procaine amide and I were different and additive. Tolamolol immediately suppressed TSRA.

Determination of plasma procainamide and N-acetylprocainamide concentration by high-pressure liquid chromatography

Determination of plasma procainamide and N-acetylprocainamide concentration by high-pressure liquid chromatography. Dutcher, John S.; Strong, John M. (Clin. Pharmacol. Cent., Northwest. Univ. Med. Sch., Chicago, Ill., USA). Clin. Chem. (Winston-Salem, N. C.), 23(7), 1318-20 (English) 1977. CODEN: CLCHAU. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) A routine method for detg. concns. of the antiarrhythmic drug procainamide (I) [51-06-9] and its active metabolite, N-acetylprocainamide [32795-44-1], in plasma is described. A simple extraction of 1.0 mL of plasma is followed by sepn. and chromatog. anal. by use of a column contg. microparticulate silica. P-Nitro-N-(2-diethylaminoethyl)benzamide hydrochloride was synthesized and used as the internal standard. Total chromatog. time is only 7 min. The day-to-day coeffs. of variation during three months of daily use were less than 4% of the mean for each compd., and no deterioration in column performance during this time was obsd. Phenobarbital, phenytoin, lidocaine, primidone, methsuximide, quinidine, and their metabolites do not interfere.