Biomedical subjects

E Ruiz-Petrich

Publications and source records attributed to E Ruiz-Petrich.

4 recordsLinked to original sources

PubMed1991

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.min-1. The components (diffusion generated and Na pump related) of the resting potential (Vr) were separated by exposure to 10(-4) M ouabain. The effects of varying the extracellular K concentration (Ko) were also examined. EXPERIMENTAL MATERIAL: New Zealand rabbits were heparinised and anaesthetised and the hearts rapidly excised and perfused in the Langendorff manner. MEASUREMENTS AND MAIN RESULTS: The membrane potential was measured with standard glass microelectrodes and the cellular content of K and Na estimated from determinations of total electrolyte and water content and volume of the inulin space of the tissue. In normoxia, Ba2+ caused a slight depolarisation at Ko below 10 mM and lengthened the action potential duration at 95% repolarisation (APD95) without altering the plateau duration. In hypoxia, Ba2+ caused further depolarisation and markedly reduced the APD95 shortening at normal Ko. The Vr v Ko relationship was considerably flattened and the diffusion component of Vr became insensitive to changes in Ko between 1.5 and 10 mM. Concomitantly, the Na pump related fraction of Vr increased under Ba2+. Barium also attenuated myocardial K loss induced by hypoxia. CONCLUSION: Our data suggest that an increase in the IK1 current underlies the maintenance of Vr in hypoxia despite the decrease in the transmembrane K gradient and contributes to the action potential shortening, speeding up the late repolarisation. The inwardly rectifying K channels would also be involved in the increased efflux of K+. In contrast, the decrease in plateau duration is probably caused by another K current system, less sensitive to Ba2+. Finally, the contribution of electrogenic Na pumping to Vr becomes critical for the maintenance of the resting potential under conditions of decreased resting permeability.

Action Potentials↗

PubMed1990

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. EXPERIMENTAL MATERIAL: New Zealand rabbits (6-7 weeks, 1.25-1.75 kg) were anesthetised and the hearts were rapidly excised and perfused with the Langendorff technique. MEASUREMENTS AND MAIN RESULTS: Standard microelectrodes were used to determine the effects of 20 mM taurine and varying Ca concentrations (from 0.3 to 5.0 mM) on action potential parameters. The resting potential was varied by changing extracellular K between 2.5 and 10 mM. Taurine significantly depolarised the membrane by about 3 mV between 5 and 10 mM Ko but not at 2.5 mM; the maximum rate of depolarisation (dV/dTmax) decreased significantly at all Ko except at 10 mM where taurine caused arrhythmias or cardiac arrest. The dV/dTmax upsilon resting potential relationship (a measure for the steady state sodium current inactivation) was not changed by taurine, but the current was depressed as a function of membrane potential, the depression being more pronounced at more positive membrane potentials. An increase in Cao from 0.3 to 5.0 mM displaced the half maximal value of the dV/dtmax upsilon resting potential relationship from -79 to -67 mV, showing that the screening effect of Ca on the negative charges at the outside surface of the membrane could be detected with this experimental approach. CONCLUSIONS: The decrease of the fast Na current by taurine can explain the arrhythmias observed at 10 mM external potassium, whereas the surface charges of the glycocalix were not affected.

Action Potentials↗

PubMed1990

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 2.46 k omega.cm2 at -65 mV to 7.30 k omega.cm2 at -30 mV. In clusters, the current-voltage relationships measured under current-clamp conditions showed anomalous rectification and the input resistance decreased from 1.05 to 0.48 M omega when external K+ concentration was increased from 6 to 100 mM. Using the model of a finite disk we determined the specific membrane resistance (12.9 k omega.cm2), the effective membrane capacity (17.8 microF/cm2), and the lumped resistivity of the disk interior (1,964 omega.cm). We conclude that 1) the voltage dependence of the specific membrane resistance cannot completely explain the membrane resistance increase that accompanies the appearance of spontaneous activity; 2) a decrease of the inwardly rectifying conductance (gk1) is mainly responsible for the increase in the specific membrane resistance and depolarization; and 3) approximately 41% of the inward-rectifying channels are electrically silent when spontaneous activity develops in explanted ventricle cells.

Animals↗

PubMed1989

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 0.1 and 4 Hz on action potential parameters were determined under control conditions and during exposure to 2 mM 4-aminopyridine, 1-3 mM CoCl2, or a mixture of 4-aminopyridine and CoCl2. The control relationship between action potential duration and pacing rate showed a maximum between 1 and 2 Hz. Under 4-aminopyridine, the plateau height and the action potential duration increased. The rate-dependent shortening of the action potential at frequencies below 1 Hz was reduced or abolished, and enhanced shortening was observed at rates above 1 Hz. Exposure to Co2+ reduced the action potential shortening at rates higher than 1 Hz. Both blockers, 4-aminopyridine and Co2+ were necessary to eliminate the rate-dependent changes of the action potential duration. Our results indicated that both the transient outward current and the inward calcium current determine the plateau height and duration for frequencies less than or equal to 2 Hz, whereas at higher rates, the Ca current plays a dominant role.

4-Aminopyridine↗