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PubMed1975

Role of catecholamines in the central mechanism of emetic response induced by peruvoside and ouabain in cats.

1 Peruvoside, (a glycoside obtained from the plant, Thevetia neriifolia Juss) and ouabain produce emesis in cats. Vomiting is not produced by these drugs in animals pretreated with catecholamine depleting drugs like reserpine, tetrabenazine or syrosingopine. Chloropromazine hydrochloride, mepyramine maleate, or BOL-148 administered intravenously or intracerebro-ventricularly do not afford protection.2 Phenoxybenzamine produces partial protection against peruvoside-induced emesis.3 Haloperidol (1 mg/kg i.v.) prevents vomiting induced by peruvoside or ouabain. Intracerebroventricularly administered haloperidol is ineffective.4 Cats pretreated with SKF-525-A, are not protected by haloperidol. Animals pretreated with phenobarbitone in a dose of 25 mg/kg for a week were protected by haloperidol, 250 mug/kg i.e. one quarter of the effective antiemetic dose in normal cats.5 It is postulated that catecholamines are involved in the mechanism of vomiting induced by cardiac gycosides. Further, a metabolite of haloperidol seems to be responsible for its effective antiemetic action.

Animals↗
PubMed1975

Cardiotonic steroids: correlation of sodium-potassium adenosine triphosphate inhibition and ion transport in vitro with inotropic activity and toxicity in dogs.

1. A new series of cardiotonics based on five steroid nuclei has been evaluated for inhibition of Na-+/K-+-ATPase and Rb uptake by red blood cells, and for inotropic activity and toxicity in dogs. Structure-activity relationships are discussed. 2. The in vitro tests can be used satisfactorily to predict inotropic activity, but not toxicity or therapeutic ratio. 3. Although compounds with greatly improved therapeutic ratios relative to ouabain and tolusin have been obtained, they proved to be strongly emetic in the conscious dog.

Adenosine Triphosphatases↗
PubMed1968

A down then up staircase in frog ventricle due to altered excitation-contraction coupling.

1. Repetitive stimulation of frog ventricle strips bathed in low calcium (< 1mM) fluids produced a decrease followed by an increase in successive tension responses which was not due to changes in the amplitude or the duration of the cardiac action potential.2. The depression of contraction reached its peak 5-10 sec after a conditioning contraction and decayed to one half in about 0.5 min; it was greater during a series of 5-10 stimuli when the frequency was increased from 3/min to 12/min.3. Lowering the external calcium concentration increased the amount of depression.4. The initial depression could be converted to facilitation by: (a) increasing the external calcium; (b) lowering the external sodium; (c) lowering the external potassium; and (d) the addition of strophanthidin.

Action Potentials↗
PubMed1969

After-effects of nerve impulses on signalling in the central nervous system of the leech.

A long-lasting hyperpolarization has been observed in sensory neurones of the C.N.S. of the leech following natural stimulation applied to their receptive fields. The underlying mechanism of this hyperpolarization and its effects on signalling were investigated by intracellular recording.1. The amplitude and duration of the hyperpolarization depended on the number of action potentials. Whereas a brief burst of impulses had little effect, a prolonged sensory discharge was followed by a hyperpolarization of up to 30 mV that gradually declined over a period of several minutes.2. The hyperpolarization was abolished by ouabain, reversibly inhibited by strophanthidin or cooling, unaffected by Mg and accompanied by an increase in membrane resistance. These observations suggest that the hyperpolarization is the result of membrane current generated by an electrogenic pump.3. A hyperpolarization similar to that recorded in the cell body also occurred in the neuronal processes within the neuropile, where synaptic contacts are made. This led to significant changes in integrative activity, such as an increase in the amplitude of excitatory synaptic potentials, a reversal of inhibitory synaptic potentials or a conduction block in parts of the neurones. All of these effects could be mimicked by injecting hyperpolarizing currents into resting cells, or abolished by injecting a depolarizing current into a cell hyperpolarized by previous impulses.4. During neuronal hyperpolarization the sensitivity of the membrane potential to small increments of external K was enhanced by a factor of about three. This effect varied with the magnitude of the hyperpolarization produced by preceding impulses and could not be mimicked by applying K to a neurone hyperpolarized by the injection of current into its cell body.5. These findings are discussed in relation to possible effects that changes in the intracellular and extracellular concentrations of ions produced by activity might have on integration in the C.N.S.

Action Potentials↗
PubMed1971

The effects of ethacrynic acid and other sulphydryl reagents on sodium fluxes in frog muscle.

1. Ethacrynic acid (2 mM) increased the sodium efflux from freshly dissected frog sartorius muscles. This increase was not observed in muscles previously treated with strophanthidin.2. In strophanthidin-treated muscles, the addition of ethacrynic acid (2 mM) caused a reduction of sodium efflux. The value of efflux reached in these muscles is similar to that observed in muscles immersed in sodium-free solutions containing strophanthidin.3. Ethacrynic acid reduced sodium influx into strophanthidin-treated muscles. Potassium influx was not affected by this substance. These findings suggest that the inhibitor blocks an exchange of sodium for sodium.4. The increase in sodium efflux caused by ethacrynic acid did not result from depolarization nor from an increase in [Na](i).5. Ethacrynic acid caused only a reduction of sodium efflux in muscles previously loaded with sodium by prolonged immersion in potassium-free solutions at low temperatures.6. A derivative of ethacrynic acid that lacks the ability to combine with sulphydryl (SH) groups did not reduce sodium efflux from muscles treated with strophanthidin.7. Para-chloromercuribenzoic acid (PCMB) reduced sodium efflux from control and strophanthidin-treated muscles. This reduction seems to be restricted to the sodium dependent component of the efflux.8. The inhibition of the sodium-dependent component of sodium efflux caused by ethacrynic acid and PCMB appears to have a similar mechanism, namely, the combination with SH groups.

Animals↗
PubMed1971

Actions of dinitrophenol and some other metabolic inhibitors on cortical neurones.

1. In cats under methoxyflurane, DNP and other metabolic inhibitors were tested on cortical neurones by iontophoresis from micropipettes.2. DNP, dinitro-o-cresol, iodoacetate, pentachlorophenol and oligomycin (uncouplers or inhibitors of oxidative phosphorylation), as well as moderate anoxia, blocked selectively and reversibly spontaneous firing and discharges evoked by ACh; responses evoked by glutamate were facilitated by moderate doses of DNP and blocked only by large amounts.3. Azide, cyanide, ouabain and strophanthidine had a mainly excitatory effect; the cardiac glycosides tended to depress more strongly responses to glutamate.4. Intracellular observations showed that DNP causes a sharp fall in electrical excitability, associated with a hyperpolarization and fall in membrane resistance.5. The hyperpolarizing action of DNP had a mean reversal level (E(DNP)) nearly 30 mV more negative than the resting potential; E(DNP) was identical with the mean reversal level for the depolarizing action of ACh, measured on the same cells.6. DNP had its usual hyperpolarizing effect on neurones whose IPSPs had been made positive by raising the internal [Cl]; the mean E(IPSP) was over 30 mV more positive than E(DNP).7. It is concluded that DNP lowers excitability by raising the membrane conductance to K(+) (g(K)) and that it blocks ACh responses selectively because ACh has a precisely opposite action on these neurones.8. In the Discussion, it is suggested that the rise in g(K) is mediated by an increase in internal free Ca(2+), caused by a slowing of mitochondrial activity, and that a similar mechanism may play a significant role in general anaesthesia.

Acetylcholine↗
PubMed1972

Inhibition of the sodium pump in squid giant axons by cardiac glycosides: dependence on extracellular ions and metabolism.

1. The rate of inhibition of the Na pump by ouabain was examined both by direct measurement of the rate of decline of the Na efflux and by the binding of [(3)H]ouabain.2. The onset of inhibition of the Na efflux was concentration-dependent; but did not follow simple first order kinetics. The time course of inhibition was roughly exponential although in about 30% of the axons inhibition was preceded by a transient stimulation of the Na efflux.3. Inhibition of the Na efflux by both ouabain and strophanthidin was apparently irreversible.4. The onset of inhibition was slowed markedly at low temperatures.5. Replacement of external Na by choline, dextrose or potassium slowed the rate of inhibition. Li behaved like Na and inhibition was faster in K-ASW than in choline-ASW.6. The rate of inhibition of Na-Na exchange was similar to that of Na-K exchange, but ouabain failed to bind securely to fully poisoned axons.7. Two components of [(3)H]ouabain-binding could be distinguished. A linear component which probably reflects uptake into the cells and a saturable component which seems to reflect binding to Na-pumping sites.8. The saturable component of binding followed a similar time course to the inhibition of the Na efflux and the rate of binding was reduced in choline-ASW and in fully poisoned axons.9. Measurements of [(3)H]ouabain-binding indicate that the number of Na pumping sites in the axon membrane is probably between 10(3) and 10(4)/mu(2).

Animals↗
PubMed1972

Effect of temperature on membrane potential and ionic fluxes in intact and dialysed barnacle muscle fibres.

1. The temperature-dependent component of the resting potential in intact, cannulated and dialysed fibres from the muscle of the barnacle Balanus nubilus was studied under a variety of different experimental conditions. A decrease in temperature from 22 to 12 degrees C produced a mean depolarization of 10 mV.2. Neither addition of strophanthidin, nor replacement of external sodium by lithium affect the voltage shift induced by temperature. However, the magnitude of the voltage shift depends on the external chloride and potassium concentration.3. The dialysis technique was applied to measure the potassium, chloride and sodium fluxes as a function of temperature. The Q(10) for the passive fluxes of these ions was 1.9, 1.7, and 1.4 respectively.4. The temperature-dependent changes in the passive ionic fluxes combined with the inability of inhibitors of the sodium pump to alter the temperature dependence of the resting potential suggest that the change induced by temperature on the resting potential is primarily caused by a change in the passive permeability ratios, and is not related to active ion transport.

Animals↗
PubMed1973

The influence of external caesium ions on potassium efflux in frog skeletal muscle.

1. At a concentration of 2.5 mM in the external solution, Cs ions reduced K efflux in muscles incubated in Na media. This effect was demonstrated in the presence or absence of 2.5 mM-K and in the presence or absence of 10(-4)M ouabain.2. In Ringer solution in which NaCl was replaced by an osmotic equivalent of MgCl(2), external Cs ions increased K efflux if the solution was K-free and decreased K efflux if the solution contained 2.5 mM-K.3. External Cs ions reduced the inward rate of leakage of Na ions into muscle cells by about 25% when the medium was K-free and contained 10(-5)M ouabain.4. The effects of 2.5 mM-K ions and 2.5 mM-Cs ions on the muscle fibre membrane potential were about the same. The influence of Cs ions on K efflux cannot be explained by changes in the resting membrane potential.5. The results suggest that a large part of the K efflux from muscle cells is mediated by a K:K exchange mechanism that is inhibited by external Cs ions.6. The results also suggest that a smaller part of the K efflux is due to K:Na exchange that is also inhibited by external Cs ions.7. In the absence of either external K or Na ions for internal K to exchange with, Cs ions promote a small amount of K exchange, perhaps via both mechanisms.

Animals↗
PubMed1973

Conductance changes, an electrogenic pump and the hyperpolarization of leech neurones following impulses.

Following trains of impulses, sensory neurones in the C.N.S. of the leech show a prolonged hyperpolarization, which lasts for seconds or minutes. In the present investigation the mechanisms that underly this hyperpolarization have been studied by recording intracellularly. Two factors have been found to be responsible. One is the activity of an electrogenic pump (see Baylor & Nicholls, 1969b); the other is a long-lasting change in K conductance.1. Additional evidence that an electrogenic pump contributes to a slow after-hyperpolarization of leech sensory neurones is provided by the effects of injecting Na intracellularly. This leads to an increase in membrane potential that is blocked by the cardiac glycoside strophanthidin. Furthermore, after a train of impulses, reducing the K concentration in the external fluid characteristically reduces the hyperpolarizing action of the pump.2. The hyperpolarization following impulses is associated with a reduction of the cell membrane resistance that can persist for several minutes.3. Several lines of evidence suggest that the reduction in input resistance during the hyperpolarization is mainly due to an increased permeability to K. Thus, when the K concentration in Ringer fluid is reduced, the peak amplitude of the hyperpolarization following a train becomes larger. Furthermore, the conductance dependent part of the after-hyperpolarization has a reversal potential close to the equilibrium potential for K (E(K)). Substitution of Cl by SO(4) has little effect either on the after-hyperpolarization or on the conductance change following a train.4. Increased external Ca concentrations lead to a marked increase in the hyperpolarization that follows impulse activity. The enhanced hyperpolarization in high Ca is associated with a corresponding reduction in input resistance. The amplitude and duration of the hyperpolarization following a brief train of impulses can be increased by a factor of 5 or more in Ringer fluid containing 10 mM-Ca instead of the usual 1.8 mM. The hyperpolarization and resistance changes still occur in solutions containing 20 mM-Mg.5. To augment the hyperpolarization the increased concentration of Ca must be present during the train of impulses.6. The relative contributions of the K conductance increase and of the electrogenic pump for generating the hyperpolarization after impulse activity are different in the three types of sensory cell responding to touch, pressure and noxious stimulation.

Animals↗
PubMed1973

The contribution of membrane hyperpolarization to adaptation and conduction block in sensory neurones of the leech.

The factors underlying sensory adaptation and conduction block have been studied in cutaneous mechanoreceptor neurones of the leech. A touch-sensitive cell was activated by applying mechanical or electrical stimuli to its receptive field on the skin. Impulses were recorded extracellularly from its axons and intracellularly from its cell body, which is situated within the C.N.S.1. Activation of the touch cell by mechanical stimuli revealed two distinct types of adaptation with characteristically different time courses. Sustained pressure on the skin caused a brief burst of impulses at the onset of the stimulus. This rapid adaptation to pressure was restricted to the part of the receptive field that had been stimulated mechanically. A second type of adaptation developed more slowly during the course of repetitive mechanical stimulation. It persisted for many seconds after the end of a train of impulses and appeared as an increase in the threshold to mechanical stimuli not only in the region of skin that had been rubbed but throughout the receptive field of the cell.2. Impulses initiated in the cell body propagated antidromically towards the skin and also raised the threshold to touch, indicating that after-effects of impulse activity were responsible for the long-lasting threshold increase.3. Repetitive mechanical stimulation could also produce a reversible conduction block in branches of the touch cell. The block occurred in discrete regions of low safety factor such as axonal branch points both within the ganglion and in the periphery. In some experiments impulses intermittently failed to reach one axonal branch yet continued to invade a separate branch of the same cell.4. Several lines of evidence indicate that both conduction block and the slow component of adaptation are linked to a prolonged hyperpolarization that follows repetitive stimulation of the touch cell. Strophanthidin, which blocks the after-hyperpolarization in touch cells, reduced the adaptation following trains of impulses and also relieved a conduction block previously established by repetitive stimulation. Furthermore, a comparison of the effects of hyperpolarizations produced by current injection and by repetitive firing showed that most of the threshold increase in the cell body after a train of impulses could be attributed directly to the membrane hyperpolarization.5. These experiments suggest several ways in which repetitive activity can have pronounced and long-lasting effects on the performance of a highly branched sensory cell. Thus a relatively small number of impulses in a touch cell can markedly decrease its sensitivity to touch. The functional role of the conduction block observed during vigorous stimulation is not as clear because activity for many seconds or minutes is usually needed to establish a block in the larger branches of the cell.

Action Potentials↗
PubMed1974

A study of the contractures induced in frog atrial trabeculae by a reduction of the bathing sodium concentration.

1. The relationship between the [Ca](o), the [Na](o) and the strength of the contracture evoked when the [Na](o) is reduced has been investigated in isolated frog atrial trabeculae.2. The strength of the contracture varies by the [Ca](o) (2) and by 4 radical([Na](o)) over the lower tension range.3. The contracture induced by reduction of [Na](o) is not sustained, but relaxes spontaneously. The rate of this relaxation is only dependent on the [Na](o) is the presence of strophanthidin.4. After the spontaneous relaxation of an Na-free contracture, the ability of the trabecula to develop tension upon a second challenge with Na-free solution returns in about 3 min if the muscle is perfused with Na-containing fluid. This recovery process is slowed if the [Na](o) is low during the recovery period, but the recovery is hastened by electrical stimulation of the preparation or by perfusion with K-free or strophanthidin containing sodium-Ringer.5. It is suggested that the influx of Ca(2+) which induces the Na-free contracture depends on the presence of Na(+) inside the cells. When the intracellular Na concentration falls, the Ca influx falls, and the muscle relaxes as a result of the activity of an intracellular relaxing structure.

Animals↗
PubMed1969

Ventricular arrhythmias related to antibiotic usage in dogs.

In dogs, pretreatment with the macrolide antibiotic tylosin (5 milligrams per day per kilogram of body weight) increased the incidence of ventricular tachycardia and fibrillation during acute myocardial ischemia. Another group received a dose of acetyl strophanthidin which was nontoxic in controls, but which resulted in a ventricular arrhythmia in six of seven animals on antibiotic treatment. Enhancement of loss of potassium ion from the myocardium by the antibiotic was presumed to be related to the altered cardiac rhythm.

Animals↗