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G Vassort

Publications and source records attributed to G Vassort.

At least 91 records · Page 5Linked to original sources
PubMed1986

A dual effect of cardiac glycosides on Ca current in single cells of frog heart.

The effects of cardiac glycosides (1 microM ouabain, 50 microM dihydrooubain, 1 microM strophanthidin) on Ca current (ICa) were investigated on Cs-loaded single frog ventricular cells using the whole-cell patch-clamp technique (9). Cardiac glycosides exert both inhibitory and stimulatory effects on ICa in 20 Cs Ringer solution, but have only a stimulatory effect in 0 Cs, when the Na,K pump is blocked. The inhibitory response seems related to the inhibition of the Na,K pump by glycosides. The stimulatory effect on ICa may contribute to the positive inotropic effect of cardiac glycosides.

Animals↗
PubMed1986

Increases in internal Ca2+ and decreases in internal H+ are induced by general anesthetics in squid axons.

Squid axons were injected with arsenazo III and treated with sea water containing compounds usually classified as general anesthetics, (pentanol-decanol and a variety of hydrocarbons and their derivatives). Such treatment led to an increase in absorbance by arsenazo III at wavelengths sensitive to [Ca]i. The effect was independent of the presence or absence of Ca++ in sea water and it was not modified by substances that release Ca from internal stores. The effect was easily reversible. In axons injected with phenol red or impaled with a glass electrode sensitive to H+, a similar treatment led to an alkalinization that was also readily reversible. Both Ca release and the change to an alkaline pH had identical time courses. The dose required for action by all of the chemical agents studied could be predicted from a knowledge of their fractional saturation in sea water, i.e. from their thermodynamic activity. For compounds with 8-10 carbon atoms, Ca-release effects can occur at concentration less than those necessary to block either conduction or Na/Ca exchange. A special chemical agent was octylamine, which induced a marked rise in pHi and in addition its nonionic form produced the typical Ca release associated with general anesthetics.

Anesthetics↗
PubMed1986

[The calcium channel: electrophysiological findings in cardiac cells].

General properties of the calcium channel are analyzed in the myocardium under voltage clamp conditions both in multicellular properties and in single isolated cells. More recently the patch-clamp has allowed us to study single channels. In normal conditions, the selectivity of the calcium channel to Ca2+ ions is very high; however, in the absence of calcium many divalent cations and even Na ions can go through this channel. Kinetic analysis shows: calcium channel inactivation depends on Ca2+ entry rather than on membrane potential, opening of this channel requires at least two transitions of closed states before the open state. Many works refer to pharmacology of the calcium channel in heart tissue. beta-adrenergic stimulation induces a large increase in current amplitude related to the increase in maximal conductance without variation in the unitary conductance. Two interpretations are available: an increase in the opening probability and/or an increase in the number of available channels, both are consecutives to phosphorylations of the channel. Cholinergic stimulation seems to have little effect. Studies of calcium antagonists have revealed that all these substances have, at various levels, use-dependent and voltage-dependent inhibitory effect. Moreover, some dihydropyridine derivatives can even, activate the channel. Antiarrhythmic as well as general anaesthetic agents have an inhibitory action on the calcium channel besides their effects on the sodium channel or the Na-Ca exchange. Very recently, the existence of another calcium conductance was demonstrated. It is characterized by a low threshold, a pure voltage-dependent inactivation, a relatively weak sensitivity to anticalcic agents and neurotransmettors.

Animals↗
PubMed1985

Role of myofibrillar creatine kinase in the relaxation of rigor tension in skinned cardiac muscle.

In the absence of creatine phosphate, MgATP produced relaxation of rigor tension in chemically-skinned right papillary muscles of the rat, the half maximal effect being obtained at 1.8 mM MgATP. In the presence of 12 mM creatine phosphate and 250 microM ADP, a decrease in MgATP concentration even to 10(-9) M never induced rigor tension. At a very low MgATP concentration (10(-6) M), the half maximal relaxing effect was obtained with 2 mM creatine phosphate, a value close to the Km of isolated MM-creatine kinase for this substrate, or with 14 microM MgADP, a value 5 times lower than the reported Km. An exogenous MgATP regenerating system (phosphoenol pyruvate + pyruvate kinase) was not able to fully relax the fibres. When MM-creatine kinase was inhibited by fluorodinitrobenzene, the dependency of rigor tension on MgATP became the same as it was without creatine phosphate. After washing out the fluorodinitrobenzene the addition of exogenous MM-creatine kinase for half an hour fully relaxed rigor tension; moreover, this effect persisted even after prolonged washout. These results show that endogenous MM-creatine kinase is able to ensure maximal efficiency of myosin ATPase by producing a localized high MgATP/MgADP ratio; they also suggest the existence of rapidly exchangeable binding sites for MM-creatine kinase in cardiac myofibrils.

Adenosine Diphosphate↗
PubMed1985

Ultrastructural changes in gap junctions associated with CO2 uncoupling in frog atrial fibres.

The correlation between gap junction morphology and the state of electrical coupling was investigated in the frog auricle, which presents an atypical gap-junction organization. Electrical uncoupling of the tissue was achieved by perfusion with CO2-saturated Ringer medium. The tissue was fixed with glutaraldehyde and freeze-fractured before and during the application of CO2-saturated Ringer medium and after returning to the initial medium. The electrical tissue coupling was assayed by microelectrode recording just before fixation. At least 97% uncoupling was induced by CO2-saturated Ringer medium, as estimated from double sucrose gap experiments on several single atrial trabeculae. Several modifications were induced by CO2-saturated Ringer medium. A decrease in the number of particles per junctional assembly and dispersion of these assemblies in the plane of the membrane, indicate a decrease in the organization of the gap junctions. In parallel, loose clusters of particles became evident on the P-fracture face of the membrane. The size of the particles in these clusters was larger than the size of the background particles, and of the gap junction particles. They never corresponded with complementary pits on the E-fracture face. On return to the initial Ringer perfusion medium the cell coupling was reversed and the gap junction dispersion was also reversed. However, the gap junctions remained small. The relationship between these morphological modifications and the conducting state of the tissue is discussed.

Action Potentials↗
PubMed1984

Calcium-mediated inactivation of the calcium conductance in cesium-loaded frog heart cells.

Ca current inactivation was investigated in frog atrial muscle under voltage-clamp conditions. To inhibit the outward currents, experiments were performed on Cs-loaded fibers and in 20 mM Cs (K-free) Ringer with 4-AP added. Inactivation, produced by a conditioning pulse, was measured by reducing the current during a subsequent test pulse. The extent of inactivation increased initially with prepulse amplitude and then decreased as the prepulse potential became progressively positive. Relative inactivation follows a U-shaped curve. When Sr was substituted for Ca, both the degree and the rate of inactivation decreased. Relative inactivation appeared to be linearly related to the amount of divalent cations (Ca and Sr) carried into the cell during the prepulse. Elevating Ca enhanced peak current and accelerated its decline. Elevating Mg decreased peak current and slowed its decline. An application of Na-free (LiCl) solution resulted in a somewhat smaller but faster inactivating current. Adrenaline increased and D600 decreased the maximal Ca conductance with little alteration in the inactivation rate; Co decreased both peak current and the rate of inactivation. Enhancement of the outward currents, reduced driving force, and intracellular surface charge screening do not adequately account for the above results. Evidence was considered that Ca entry mediates most of Ca current inactivation in frog atrial fibers. Removal from inactivation was also investigated in normal-Ca, Ca-rich, and Sr solutions. Recovery after partial inactivation by high depolarization was biphasic. Recovery was slowed by 10 Ca and accelerated by 1.8 Sr, whereas opposite effects have been shown on activation.

Animals↗
PubMed1984

Changes in external Na induce a membrane current related to the Na-Ca exchange in cesium-loaded frog heart cells.

The effects of transient alterations in Nao were investigated under voltage clamp conditions in frog heart cells previously loaded with Cs. Tetrodotoxin and Cs were used to inhibit Na and K currents. On applying a Na-poor solution (39.2 mM), an outward current was generated during both depolarizations and hyperpolarizations. The current amplitude described a U-shaped function of the membrane potential. On reapplying the standard solution after 15 min equilibration, an inward current was then induced that exhibited a bell-shaped function of the membrane potential. Current amplitude was sensitive to the external Ca concentration. Increasing pHi by 10 mM NH4Cl enhanced this current, while the internal acidification that occurred on switching back to the control solution greatly reduced it. Variations in the amplitude of this current during repetitive stimulations or long pauses are best explained by subsequent alterations in Nai and pHi; no evidence for a time dependence was found. This current was inhibited by La3+, Co2+, and D600, and was sensitive to adriamycin, quinidine, and disopyramide; lidocaine, another local anesthetic, and nifedipine had no effect. These observations extend previous work on intact heart cells and sarcolemmal vesicles. They suggest that the Na-Ca exchange may generate a current that is outward when Ca ions are moving into the cell.

Amiloride↗
PubMed1983

Role of cyclic nucleotides and energy-rich phosphates during energetic deficiency in frog heart.

Mechanical performance, energy-rich phosphates and cyclic nucleotides of frog heart were measured during energetic deficiency and subsequent addition of adrenaline. When oxidative metabolism was inhibited by 3 mM cyanide, tension decrease was accompanied by a decrease in creatine phosphate while ATP and cyclic nucleotides did not vary significantly. After subsequent addition of adrenaline mechanical activity remained less than control value; creatine phosphate (CP) concentration was further decreased while cAMP was increased in the same proportion as when adrenaline alone was added. In the presence of cyanide, the weak inotropic effect of adrenaline is not due to an alteration of cyclic nucleotides but is rather correlated to a further decrease in energy-rich phosphates, mainly in creatine phosphate. These results suggest that creatine phosphate may control contractile activity and may be a limiting factor for inotropic interventions at least during energetic inhibition.

Adenosine Triphosphate↗
PubMed1983

Effects of internal sodium and hydrogen ions and of external calcium ions and membrane potential on calcium entry in squid axons.

Squid giant axons were impaled with electrodes to measure pNai, pHi, Em, and were injected with either aequorin or arsenazo III to measure [Ca]i or with phenol red to measure [H]i. Depolarization of such axons with elevated [K] in sea water leads to a Ca entry that is a function of [Ca]o, [Na]i, and [H]i. With saturating [Na]i half-maximal Ca entry is produced by a [Ca]o of 0.58 mM. With saturating [Ca]o, depolarization produced by 450 mM-K+ leads to half-maximal Ca entry when [Na]i is 25 mM; entry is virtually undetectable if [Na]i is 18 mM. If [Ca]o is 50 mM, Ca entry upon depolarization as measured with aequorin is phasic with a rapid phase of light emission and a plateau; Ca entry as measured with arsenazo III shows no such phasic behaviour, absorbance vs. time is a square wave that closely follows the depolarization vs. time trace. Both detectors of [Ca]i show a square-wave response if [Ca]o is 3 mM. The introduction of 2 mM-CN into the sea water bathing the axon does not affect the response to depolarization nor does the destruction of most of the ATP in the axon following the injection of apyrase. If axons are microinjected with phenol red rather than arsenazo, the entry of Ca produces an acidification in the peripheral parts of the axoplasm. Other experiments measuring [Ca]i show that Ca entry is strongly inhibited by a decrease in pHi. Making sea water alkaline with pH buffers scarcely affects the Ca entry induced by depolarization; making axoplasm alkaline by adding NH4+ to sea water greatly enhances Ca entry by Na/Ca exchange and also enhances the ability of axoplasmic buffers to absorb Ca.

Aequorin↗
PubMed1983

[Ionic bases of cardioplegic solutions. I. Some implications of the role of ionic equilibrium in the preservation of cardiac metabolism. Experimental study of hypoxia and calcium overloads].

The importance of respecting the ionic equilibrium of cardioplegic solutions was studied experimentally in rat papillary muscle by observing the mechanical and metabolic changes after altering the ionic composition of the washing fluid. The first part of the study demonstrated the nature of the "rigor" of sustained tension induced by the inhibition of the respiratory activity of the mitochondria: this observation showed that this tension was essentially related to the energy deficit induced by poisoning. In the second part, it was shown that calcium overload induced by changing the ionic composition of the nutrient fluid (replacing some of the Na+ ions by K+ or Li+), that is to say related to dysfunction of the Na+-Ca++ exchange induced a contraction which also rapidly evolved to a tension of rigor. This effect was accompanied by a significant reduction in the adenosine triphosphate (ATP) and creatine phosphate (CP) content. The mechanical consequences of prolonged hypoxia or calcium overload are directly related to the reduction in energy reserves producing a marked deficit of ATP in the myofibrils, and resulting in a stable but reversible increase in cardiac muscle rigidity (or rigor). The prevention of calcium overload during the use of cardioplegic solutions is discussed in the context of metabolic myocardial protection. The inhibitory substances of calcium influx such as the calcium antagonist drugs or Mg++ may have an important role to play, in addition to the maintenance of ionic concentrations, especially that of sodium, close to those of the external fluid.

Adenosine Triphosphate↗
PubMed1982

Participation of the sarcolemma in the control of relaxation of the mammalian heart during perinatal development.

Stereological measurement of cell diameter and cell surface-to-volume ratio (S/V) were compared in fetal, newborn, and adult rabbit and frog hearts. In the frog heart, S/V was high (1.32 micron-1), comparable to that of the fetal rabbit heart (1.03 micron-1). Only 8 days after birth, cell diameter increased while S/V progressively decreased towards the adult value of 0.30 micron-1. The possible implications of the S/V decrease were investigated on the relaxation of cardiac contraction. Unlike the relaxation of the adult mammalian heart, but like that of the frog, relaxation of the fetal heart was sensitive to a reduction of Na+-Ca2+ exchange by a low-Na+ medium. With perinatal development, the participation of Na+-Ca2+ exchange in relaxation decreased and was progressively masked by the sarcoplasmic reticulum and/or other systems.

Animals↗
PubMed1981

The electrogenic Na-Ca exchange and the cardiac electrical activity. I--Simulation on Purkinje fibre action potential.

1. The effects of the current (iex) generated by the Na-Ca exchange mechanism have been investigated on the electrical activity of a cardiac cell using the model of MC ALLISTER et al. (1975) for the Purkinje fibre action potential (AP). 2. The reversal potential and the steady-state value of iex were described by the same equations as for the squid axon (MULLINS, 1976). The maximal intensity and the time constant of iex were extrapolated from experiments using frog hearts. 3. A compact program written with the Adams method in Fortran IV (PLANT, 1979) allowed a minicomputer to be used. 4. The addition of iex to the previous model induced a prolongation of the AP and a reduction of the duration of the diastolic phase. 5. Increasing the maximal steady-state amplitude of iex may lead to early after depolarizations and oscillatory behaviour. These effects can be prevented by adequate changes in the amplitude of some potassium outward currents. 6. It is concluded that : (i) alterations of the Na-Ca exchange, e.g., by cellular Na loading, should induce variations of both AP repolarization and diastolic phase durations and, consequently, alter the beating rate ; (ii) iex could interfere with the outward currents whose characteristics should be reconsidered.

Action Potentials↗
PubMed1980

The hypodynamic state of the frog heart. Further evidence for a phosphocreatine-creatine pathway.

The hypodynamic state of frog heart has been investigated from the energetic point of view. The amplitude of tension was enhanced when the oxidative metabolism was stimulated by oxygen and pyruvate. However, a time-dependent tension decrease still occurred with both oxygen and pyruvate. Hypodynamia, although slowed down under these conditions, was accompanied by a decrease in CP rather than in ATP. It is shown that the decrease in CP was due to a leak of creatine out of the cell, consequent to the non-equilibration of the oncotic pressure in the perfusion fluid. Creatine (20 mM) or any plasma expander, prevented the fall in both CP and tension. These results are in agreement with the proposal that the CP/CK/Cr system is the major metabolic intermediate between production and use of energy for contraction and that, besides Ca ions, it participates in the regulation of tension. It is suggested that hypodynamia mostly originates in a decreased Ca utilization due to shortage of energy.

Animals↗