Biomedical subjects

L Cedrini

Publications and source records attributed to L Cedrini.

18 recordsLinked to original sources

PubMed1988

The effects of gaboon viper (Bitis gabonica) venom on voltage-clamped single heart cells.

The effects of crude B. gabonica venom on single ventricular myocytes from guinea-pig hearts were studied using the patch clamp technique in the 'whole cell' mode. Irreversible effects on the membrane currents, which became prominent within 15 min of venom application, were: (1) a decrease in the time invariant current (associated with the inward rectifying K+ current), most clearly seen over a voltage range negative to the resting membrane potential; and (2) a decrease in the peak inward current (associated with the Ca2+ current) elicited by steplike depolarizations from a holding potential of -40 mV. A transient increase in the peak inward current, which preceded its eventual decline, was also noticed; it peaked 6-10 min after the venom was applied. Application of the venom to unclamped, stimulated cells resulted in a shortening of the plateau phase and disturbances of the repolarization phase of action potentials. An early transient prolongation and elevation of the plateau was observed, occurring with the same time course of the transient increase in the peak inward current. No signs of damage to the cell membrane integrity, neither electrical (appearance of a leakage current) nor morphological (surface blebs, loss of striation pattern and of rodlike shape in the isolated myocytes), accompanied the effects observed on ionic currents and action potential activity, supporting the hypothesis of a selective cardiotoxic action of B. gabonica venom.

Action Potentials↗

PubMed1986

The effects of Gaboon viper (Bitis gabonica) venom on the electrical and mechanical activity of the guinea-pig myocardium.

The effects of Bitis gabonica venom were tested on guinea-pig heart, using both Langendorff preparations and isolated atrial strips or papillary muscles. In the self-paced whole heart, a single passage of 50 micrograms of venom per ml produced in sequence: irregularities of the A-V conduction and decrease of the contractile strength, progressive failure to relax and systolic arrest of the heart. Pretreatment with atropine reduced but did not abolish these effects. Venom recycled through the heart was effective at a much lower dose. The relationship between resting membrane potential and [K+]o was unaffected by envenomation, suggesting that the action of the venom cannot be ascribed to a loss of ionic selectivity of the cell membrane. The peak amplitude of action potentials declined in papillary muscle exposed to venom at physiological [K+]o, while in atrial cells it was affected only at higher [K+]o. Maximum upstroke rate of the action potential vs. resting potential at different [K+]o gave a sigmoid relationship, characterized by a higher upper asymptote as compared to controls, and by a shift of the curve towards more negative voltage values. A marked shortening of the action potential duration, paralleled by a decrease in time to peak tension, was recorded as well. 'Slow' action potentials, elicited in 20 mM K+ solution, were completely abolished within 10 min of perfusion with venom. These results are consistent with the hypothesis that the venom interacts with both transmembrane Ca2+ inflow and Ca2+ binding at the external side of the cell membrane. A transient positive inotropic effect induced by the venom was observed in papillary muscle and in atropinized atrium. This effect was abolished by previous administration of reserpine to the animal or by addition of propranolol to the perfusing solution, suggesting a venom-induced release of both adrenergic and cholinergic transmitters from nerve endings within the cardiac tissue.

Action Potentials↗

PubMed1984

[Postnatal variations in the electrophysiological characteristics of the mouse heart].

Electrocardiograms were recorded in 13 mice, from birth up to 57 days of age; during this period the heart rate, at rest, showed a marked increase (from 310 to 797 beats/min), occurring in two waves. Recordings of the intracellular electrical activity in the atria disclosed a different temperature dependence of the resting membrane potential, action potential duration and Vmax in the neonatal mouse as compared with the adult one. The results are consistent with the suggestion that a decrease of the 'slow inward' conductance/K+ outward conductance ratio still occurs during a postnatal period.

Action Potentials↗

PubMed1981

Calcium-dependent action potentials elicited in the lizard ventricle by a prolonged hypothermic incubation.

After a prolonged hypothermic incubation (48 h at 4 degrees C), lizard ventricles perfused with a solution containing 15 mM k+ and 1 mM Ca2+ exhibit slow responses, which are similar (prescinding from their noticeable greater duration) to the responses which can be elicited, in the same depolarizing solution, by increasing the external calcium concentration or by adding catecholamines to the perfusing medium. The phenomenon is transient, and vanishes within 90 min from the end of the hypothermia.

Action Potentials↗

PubMed1981

Effect of Bitis gabonica venom on the action potentials of guinea-pig heart. Preliminary results.

The effect exerted by different doses (50 to 500 mg/kg body weight, or 1 or perfusing solution) of the lyophilised secretion of B. gabonica venom glands has been studied -by intracellular electrodes- on the electrical activity of atrial and ventricular cells from guinea-pigs hearts, by using both open-chested animals and isolated preparations. Noticeable changes in the features and duration of the repolarization phase of the action potentials precede the abolition (reversible, after washing) of the contractile activity. No significant changes of the diastolic potentials have been evidenced in the preparations perfused in vitro.

Action Potentials↗

PubMed1981

Contraction features in normal and hypodynamic lizard ventricle.

Isometric twitches and intra- and extracellular electrical activity were recorded at various driving rates from lizard ventricles, either in the normal inotropic state, or in a hypodynamic state induced by perfusing at a high flow rate for a long time. Electron micrographs were obtained from hearts fixed immediately after dissection and from preparations perfused in vitro for various periods. It was found that the peak of the steady-state strength-interval relationship shifts towards higher stimulation rates with the development of hypodynamia. Such a change is similar to that induced in normal preparations by perfusing with calcium-poor solutions. The normal strength-interval relationship can be restored in hypodynamic preparations by perfusion with a calcium-rich solution. Also, in the hypodynamic state, the action potential duration is increased and (+ dP/dt)max is decreased, while the shape of the staircases at various stimulation rates is modified. These changes occur in the presence of well-preserved ultrastructural features of the preparation. The results suggest that the twitch tension results from the contribution of two Ca ions fluxes: an early one from a cellular store, and a late one related to the action potential duration. The ultrastructural findings are consistent with the hypothesis that a store, from which a rapid release of calcium occurs, exists in the lizard ventricle. A hypodynamic state would be caused by a reduced calcium affinity of such store, and by a decreased Ca++ influx during the action potential plateau.

Action Potentials↗

PubMed1980

Staircase in lizard ventricle. I. Time-course analysis in the normal inotropic state.

The staircases drawn by the isometric twitches up to the attainment of the steady-state at frequencies in the range of 1 to 60 min-1 have been studied in superfused half-ventricles of lizard, showing a normal inotropic state. The differences between the instantaneous twitch tension and the steady-state value has proved to be fitted by the algebraic sum of 3 or 4 exponential phases. The analysis of the electrical and mechanical activity of the preparation suggests a correlation between each exponential contribution to the staircase profile and the changes of the action potential duration as well as of the balance between the two sources (transmembrane influx and impulsive release from an intra or extracellular store) of calcium ions activating the contraction.

Animals↗

PubMed1980

Staircase in lizard ventricle. II. Time-course analysis in the hypodynamic state.

The analysis of the staircases in lizard ventricle, that was the object of the preceding paper, has been extended to the hypodynamic condition, induced by the prolonged perfusion of the ventricular preparation at high flow rate. For comparison, the effects of lowered [Ca]0 on the normal ventricle as well as of raised [Ca]0 on the hypodynamic ventricle have been also investigated. The results show that the low rate (less than or equal to 2 min-1) staircase in hypodynamic condition is formally described by the same algebraic sum of exponentials as in normal hearts: Pt - Ps - - phi 1 - phi 2 + phi 5, although with altered values of both their extrapolations P' at the time t0 and their time constants tau. On the contrary, t high beat rates the staircase profiles obey to the the eqn.: Pt - Ps = - phi 2 + phi 3 - phi 4 + phi 5, which is characterized by the absence of the phi 1 component, as well as by the occurrence of the phi 4 component, that fits to an early phase of rapid build-up of the isometric twitch tension from the reduced values of the hypodynamic "rested state contraction'. A two-fold increase of the [Ca]0 approaches the time-course of the hypodynamic staircases, whether at low or at high beat rate, to that displayed by the ventricles in normal inotropic state. The results are discussed on the assumption of the double-source hypothesis for the Ca that activates the contraction in the lizard ventricular cells.

Animals↗

PubMed1980

On the reversal of the heart hypodynamia by means of a prolonged cooling.

Lizard ventricles induced to hypodynamia by the high flow rate of the perfusing solution were submitted either to brief periods of cooling (from 20 to 25 degrees C), or to a prolonged hypothermic incubation (35 h at 4 degrees C) followed by a recovery at room (20 degrees C) or reduced (15 degrees C) temperature. Isometric rested state contractions as well as staircases and steady-state twitches at 20 or 4 min-1 were recorded. While a brief exposure to reduced temperature proved to increase the peak tension of the twitches, without altering the peculiar tension-frequency relation and the pattern of the staircases which characterize the hypodynamic condition, a transitory post-effect of the prolonged hypothermic incubation was noticed, that causes the reappearance of the contractility features which characterize the normal inotropic state. The results are discussed in the light of the double-component hypothesis for the twitch in lizard ventricular cells, and interpreted as evidences that a brief exposure to low temperatures enhances the transmembrane Ca++ influx during the AP, that causes an augmentation of the late, slow rising component of the twitch; while the prolonged hypothermic incubation would cause also an increase of the Ca++ content in a cellular store, and consequently a potentiation of the early, impulsive component of the twitch.

Animals↗

PubMed1979

Effect of temperature on the electrical and mechanical activity of lizard ventricular myocardium.

Intracellular action potentials and isometric twitches were recorded from lizard ventricles electrically driven at 20 and 4 beats/min and submitted to temperatures changes between 10.5 and 21 degrees C. It was found that cooling induced a depolarization of the diastolic membrane potential ER, which below 15 degrees C exceeded that predictable for a diffusion potential; on the contrary, during the recovery from hypothermia ER underwent a transitory hyperpolarization. Other effects of the low temperature were a decrease of the maximum rate of depolarization, a lengthening of both the action potential duration and the time to peak contraction, an increase of the strength of contraction, in the hearts driven at 20/min it became apparent also an increase of the action potential overshoot. The hypothesis is discussed that the positive inotropic effect of low temperatures may be due not only to a slowing down of the repolarization of the action potential, but also to an increase of the slow inward current intensity.

Action Potentials↗

PubMed1979

Acetylcholine's inhibitory effect on the calcium-dependent depolarization in the heart cells of a reptile (Lacerta sicula campestris). Preliminary notes.

The results of experiments performed with high - K+ solutions suggest that in the lizard atrial cells Ach normally displays its negative inotropic effects by a double mechanism = an "indirect" inhibition, mediated by the increase of the membrane permeability to K+ ions; and a "direct" inhibition of the Ca- carried slow inward current. In the ventricular fibres there isn't a direct-effect of this drug, under normal conditions.

Acetylcholine↗

PubMed1973