Magnesium: effects on reperfusion arrhythmias and membrane potential in isolated rat hearts.

The effects of Mg2+ concentration (Mg2+o, 0, 1.2, 2.4, and 4.

Modulation of the electrophysiological effects of ischemia reperfusion by methylisobutyl amiloride.

We studied the effect of the Na+/H+ exchanger inhibitor methylisobutyl amiloride (MIA, 1 microM) on action potential characteristics and arrhythmias induced by: (a) reperfusion following regional ischemia in rat hearts and (b) realkalization after lactate acidosis in rabbit hearts. We also determined the effect of MIA on the incidence of transient inward currents (ITIs) induced by acidosis-realkalization in rabbit cardiocytes. Ligation of the LAD coronary artery for 10 min depolarized the resting potential from -78 +/- 1.

Early action potential shortening in hypoxic hearts: role of chloride current(s) mediated by catecholamine release.

We tested the hypothesis that the early action potential shortening induced by hypoxia in perfused hearts is attributable to chloride currents activated or modulated by endogenous catecholamine release. Rabbit hearts perfused at 33 degrees C and paced at 2.5-2.

Partial contribution of the ATP-sensitive K+ current to the effects of mild metabolic depression in rabbit myocardium.

The object of the study was to compare the capability of glibenclamide to block the effects of K(+)-ATP channel activators on action potential duration and steady state whole cell current to its efficiency in counteracting the effects of hypoxia or metabolic poisons in the presence of glycolytic substrate. The modulation of action potential duration by 30 microM glibenclamide was tested in perfused hearts subjected to hypoxia or to the K(+)-ATP channel opener pinacidil. Similar protocols were used to study the modifications of the steady state whole cell current in isolated ventricular myocytes.

Effects of K+ channel blockers on the action potential of hypoxic rabbit myocardium.

1. In order to assess the role of different ionic currents in hypoxia-induced action potential shortening, we investigated the effects of blockers of voltage-dependent and ATP-sensitive K(+)-channel on the membrane potential of hypoxic rabbit hearts and papillary muscles. The response to blocking of the inward rectifier was studied at three external K+ concentration: 2.

Role of the inward rectifier IK1 in the myocardial response to hypoxia.

Study Objective: The aim was to assess the contribution of the inward rectifier IK1 to the electrical responses of the myocardium to hypoxia: action potential shortening, maintenance of resting potential, and myocardial K loss.

Design: Hypoxia induced changes of gK1 were inferred from the effects of 40 microns Ba2+ on action potential duration, resting potential, and cellular K content of normoxic and hypoxic rabbit hearts paced at 2.5 Hz and perfused at 33 degrees C and constant coronary flow of 20 ml.

Taurine depresses INa and depolarises the membrane but does not affect membrane surface charges in perfused rabbit hearts.

Study Objective: The aim was to determine whether taurine influences the membrane surface charges in cardiac muscle.

Design: Screening of the negative charges at the outside surface of the membrane results in a shift of the steady state inactivation of the sodium system towards less negative potentials. This feature was used to study eventual effects of taurine on surface charges and the data were compared to the known influence of varying extracellular calcium.

Membrane resistance increases when automaticity develops in explanted rat heart cells.

We compared the passive electrical properties of isolated ventricular myocytes (resting potential -65 mV, fast action potentials, and no spontaneous activity) with those of 2- to 7-day-old cultured ventricle cells from neonatal rats (resting potential -50 mV, slow action potentials, and presence of spontaneous activity). In myocytes the specific membrane capacity was 0.99 microF/cm2, and the specific membrane resistance increased from 2.

The mechanism of the rate-dependent changes of the conducted action potential in rabbit ventricle.

Blockers of the transient outward current (4-aminopyridine) and the Ca current (Co2+) as well as injection of polarizing current during the plateau were used to assess the role of these current systems as determinants of action potential duration at different pacing rates. Papillary muscles and ventricular trabecula were superfused with oxygenated Krebs solution at 33 degrees C and driven at a basic rate of 1 Hz. The effects of varying the frequency of stimulation between 0.