These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Effects of BW A256C, a novel class 1 antiarrhythmic agent, on maximum rate of depolarisation of cardiac action potentials in vitro: frequency, use, and voltage dependence.
    Author: Donoghue S, Payne PN, Allan G.
    Journal: J Cardiovasc Pharmacol; 1987 Jan; 9(1):12-8. PubMed ID: 2434786.
    Abstract:
    The frequency, use, and voltage-dependence of the effects of a novel antiarrhythmic agent, BW A256C, on the maximum rate of depolarization (Vmax) of action potentials in guinea-pig right ventricle were studied using standard microelectrode recording techniques in vitro. BW A256C (10(-6) M) reduced Vmax in a frequency-dependent way in the range 0.33-3.3 Hz; the maximum reduction was at the highest frequency. BW A256C did not cause resting block of Vmax. The onset of use-dependent Vmax reduction at 3.3 Hz followed a monoexponential function with a very slow rate constant, 0.019 +/- 0.003 AP-1. The recovery from use-dependent reduction, studied by applying single extra stimuli at various times after trains of stimuli at 3.3 Hz, was also very slow; half-life (t 1/2) for recovery was 119.0 +/- 19.2 s, and the time constant tre was 171.7 +/- 27.7 s. For comparison, the values for Flecainide (10(-5) M), obtained under identical conditions, were: rateon, 0.106 +/- 0.010 AP-1; t 1/2, 7.68 +/- 0.20 s; tre 11.07 +/- 0.29 s (means +/- SEM). In the presence of BW A256C (10(-6) M), the normalised diastolic membrane potential-Vmax curve was significantly shifted in the hyperpolarizing direction. The mean shift was 5.5 +/- 1.1 mV, measured at the 50% reduction of Vmax level. BW A256C is therefore classified as a novel "slow" class 1C antiarrhythmic agent.
    [Abstract] [Full Text] [Related] [New Search]