Search PubMed⌕ Search

Biomedical subjects

E Coraboeuf

Publications and source records attributed to E Coraboeuf.

126 records · Page 7Linked to original sources
PubMedDate not supplied

Effects of potassium conductance inhibitors on spontaneous diastolic depolarization and abnormal automaticity in human atrial fibers.

The capability of generating spontaneous diastolic depolarization and automaticity was investigated in vitro by means of standard microelectrode techniques in 50 human atrial preparations. Samples were classified within two groups: group 1 was composed of 12 well-polarized preparations exhibiting action potentials that were fast responses (mean maximum diastolic potential: -75.5 mV and Vmax greater than 100 V/s); group 2 was composed of 38 partially-depolarized samples (mean maximum diastolic potential: -50.3 mV and Vmax less than 10 V/s) and was further divided into two subgroups. Subgroup 2A consisted of 20 spontaneously beating preparations and subgroup 2B consisted of 18 non-automatic partially-depolarized specimens. Highly-polarized fibers from group 1, although exhibiting a slight diastolic depolarization which was almost entirely suppressed by 2 mM caesium, never presented spontaneous activity under our experimental conditions. 90% of automatic fibers from subgroup 2A were sampled from dilated atria. In automatic preparations, diastolic depolarization was usually separated into two phases: an initial phase, also present in non-automatic fibers, and a late phase. Changes in the initial phase were not accompanied by concomitant changes in the spontaneous rate. Abnormal automaticity was clearly related to the late diastolic phase (absent in non-automatic fibers), the generation of which appeared to be a specific property of automatic fibers. The use of K conductance inhibitors (caesium, 4-aminopyridine, barium, low K solutions) provided indirect evidence that neither delayed outward ix current nor if type inward current are principally responsible for abnormal automaticity.

4-Aminopyridine↗
PubMedDate not supplied

Effects of excess free fatty acids on the electrophysiological properties of ventricular specialized conducting tissue: a comparative study between the sheep and the dog.

The effects of sodium palmitate were studied on the transmembrane potential properties of canine subendocardial Purkinje fibers and on the Purkinje fibers of the dog and the sheep false tendons with standard microelectrode technique. Following 4 h of superfusion with palmitate/albumin = 10, action potential duration in all preparations was prolonged (p less than 0.05), and resting membrane potential, action potential amplitude, and maximum rate of rise were slightly but significantly (p less than 0.05) diminished in the subendocardial preparation, but not in the false tendons. Action potential prolongation was reversible in the dog preparations but only partially reversible in the sheep Purkinje fibers. Following palmitate-induced prolongation of the action potential duration, rapid spontaneous diastolic depolarization was observed in the subendocardial Purkinje fibers. Palmitate enhanced spontaneous diastolic depolarization in the sheep but not in the dog Purkinje fibers (false tendons). Albumin alone had no effect on all action potential properties in both species. It is concluded that extended periods of exposure of the ventricular specialized conducting tissue to excess levels of palmitate can induce action potential abnormalities and subsequent rhythm disturbances both in the dog and the sheep.

Action Potentials↗
PubMedDate not supplied

[Abnormalities of ion movements in cardiac hypertrophy and failure].

Main sources of transmembrane ionic current that lead to cellular electrical activity are described. In hypertrophied myocardium, action potentials are usually markedly prolonged. Current modifications that could be responsible for this are not well established. However, despite divergent observations, one can postulate that calcium current density (current per area unit) is maintained to its normal level and that action potential lengthening can be related to a prolonged Na-Ca exchange current, a prolongation due to the lengthening of the calcium transient (systolic increase of intracellular calcium). In heart failure, calcium current appears reduced. It is markedly depressed in dilated human atria which greatly shortens action potential plateau. In cat, during the initial overload phase which triggers right ventricle hypertrophy, action potential plateau is also transiently reduced, which could correspond to an initial reduction of calcium current before its normalisation. Several effects are probably related to fiber stretch and appear to involve different types of stretch sensitive ionic channels.

Action Potentials↗
PubMedDate not supplied

Ionic basis of excitation mechanism in cardiac muscle.

Cardiac electrical activity is due to passive ionic permeabilities and, partially, to nonneutral (electrogenic) active transport, but extracellular accumulation or depletion of potassium is also of importance. The rapid sodium current responsible for the spike of the action potential and the slow calcium or calcium and sodium inward current responsible for the plateau are governed by activation and inactivation variables, but the range of potential in which the corresponding conductances "open" or "close" differs markedly. For that reason, partially depolarized fibers exhibit slow action potentials deprived of a rapid ascending phase. The normal sinoatrial and atrioventricular node action potentials are of this type. Several components of of outward (repolarizing) currents, mainly carried by potassium ions (although anions may also carry repolarizing currents), exist, some of them being controlled by intracellular calcium. Repolarization is a much more labile process in Purkinje fibers than in myocardium. Recovery from inactivation of rapid and slow inward currents is important in controlling the shape of the action potential as a function of the previous diastole.

Action Potentials↗
PubMedDate not supplied

[Electrogenic sodium-calcium exchange and electrical activity in cardiac cells].

Several studies have shown that the Na-Ca exchange is electrogenic in cardiac tissues and that the current carried by the exchange, iNa-Ca, participates in the development of the cardiac action potential plateau. The aim of the present study was to assess the contribution of iNa-Ca to the development of the plateau in different preparations, i.e. normal and hypertrophied (DOCA-salt) perfused rat hearts, normal and dilated (MS 200 strain) perfused hamster hearts and normal human atrial myocytes and to examine the repercussion of iNa-Ca suppression on the global electrogram of the perfused guinea-pig heart. iNa-Ca was suppressed by briefly substituting lithium for sodium (Li test). In the normal rat heart, the Li test resulted in a depression of the late component of the plateau. In the severely hypertrophied rat heart, the action potential was lengthened, the two components of the plateau barely distinguishable. The part of the plateau suppressed during Li perfusion was not larger in amplitude than in the normal rat heart, but was of much longer duration. In the dilated heart of hamsters older than 60 days of age the shortening effect of the Li test was much larger than in the normal hamster heart indicating a strongly increased contribution of iNa-Ca to the plateau development during dilatation. The contribution of iNa-Ca to the action potential plateau of human atrial myocytes was as large as that found in animal ventricles and varied with the type of cell studied. In the perfused guinea-pig heart the Li test resulted in a sizeable shortening of QT duration and a marked decrease in T wave amplitude suggesting that iNa-Ca may be a major source of current in the building up of the ventricular complex of the electrocardiogram in normal and pathological conditions.

Action Potentials↗