Search PubMed⌕ Search

Biomedical subjects

E Varga

Publications and source records attributed to E Varga.

At least 127 records · Page 7Linked to original sources
PubMed1979

Hallucinations.

Explore the source record for details and available documents.

Attention Deficit Disorder with Hyperactivity↗
PubMed1979

The 24Na-transport increasing effect of veratrine in frog sartorius muscle influenced by the tonicity, composition and temperature of the external environment.

The influence of tonicity, ionic composition and temperature of the incubating medium on the increasing effect of veratrine on 24Na transport in the frog sartorius muscle has been studied. (1) The effect of veratrine applied during 24Na loading on the rate coefficient for sodium loss depended on the tonicity of the medium. The rate of loss of 24Na from muscles loaded in the presence of veratrine was not affected if the muscles had been equilibrated in hypertonic medium. However, when treating the muscles with veratrine in isotonic medium during 24Na loading, we obtained a twofold increase in the rate coefficient for sodium loss. (2) The effect of veratrine applied during the desaturation period on 24Na efflux was also found to depend on the tonicity of the medium. Veratrine applied during the desaturation period increased the 24Na efflux in muscles equilibrated in isotonic Ringer's solution. However, when the muscles were equilibrated in hypertonic medium, veratrine did not influence 24Na efflux, not even after the rate of 24Na loss had been decreased by ouabain. (3) Hypertonic medium inhibited the Li uptake-enhancing effect of veratrine, while in isotonic medium veratrine had a marked enhancing effect. (4) In hypertonic medium lithium inhibited the otherwise characteristic increasing effect of veratrine on 24 Na uptake. (5) The increase of intracellular sodium concentration as a result of incubation in cold, potassium-free Ringer's solution did not influence the 24Na exchange-increasing effect of veratrine in isotonic medium. (6) The increasing effects of 0.1 and 0.5 mM veratrine on 24Na influx had the same degree at room temperature. However, at 5 degrees C 0.5 mM veratrine increased 24Na influx to a greater extent than 0.1 mM. (7) On the basis of our earlier experiments it has been suggested that the site of action of the 24Na uptake-increasing effect of veratrine could be the neural structures in the muscle equilibrated in hypertonic media. The present experiments confirm this suggestion and at the same time demonstrate that there are substantial differences in the mechanism of the sodium transport of veratrine-treated neural and muscle membranes, which become more apparent in hypertonic medium.

Animals↗
PubMed1978

Tardive dyskinesia and psychotropic drug history.

The adult population of a large mental hospital was screened for tardive dyskinesia (TD). Approximately 11% of the hospital population showed signs of TD; females and the elderly were over-represented in the TD group. A representative sample of those with TD was selected and a control (non-TD) patient was chosen to match each of the TD subjects in age, sex, length of hospitalization, diagnosis, and race. The charts of these subjects were searched for any indices of brain damage and the complete psychotropic medication history was recorded. There was no difference between the TD and controls in the amount of psychotropics ingested, in the duration of administration, in the kinds of drugs, or in the organicity history. Women as a group, however, tended to have more polypharmacy than men. The role of neuroleptics in TD is discussed as well as other possible etiological factors.

Adult↗
PubMed1978

Effect of inhibitors of aerobic and anaerobic metabolism on the membrane potential oscillation induced by veratrine.

1. Veratrine-induced membrane potential oscillation is still apparent after the muscle has been treated with 1 mM KCN, or 1 mM NaN3, or 0.2 mM DNP, to inhibit oxidative metabolism. 2. The frequency of the membrane potential oscillation decreases reversibly in response to 1 mM phlorrhizin either in Na- or Li-Ringer solution. 3. Veratrine causes no membrane potential oscillation but only depolarization in muscles pretreated with 0.5 mM iodoacetic acid, eventually a few abortive waves can be observed. Iodoacetic acid also abolishes oscillation which has already developed. 4. On the basis of the present data it is suggested that rhythmic changes of metabolism may be related to the oscillation of membrane potential.

Aerobiosis↗
PubMed1978

The effect of veratrine on 24Na uptake by frog sartorius muscle in hypertonic media.

The effect of veratrine on 24Na uptake by sartorius muscles incubated in hypertonic media has been studied. 1. 0.1 mM veratrine increases 24Na uptake in muscles incubated even in different hypertonic solutions (normal Ringer + 300 mM sucrose or glucose or 150 mM NaCl). 2. 0.05 mM curare inhibits the 24Na uptake increasing effect of veratrine in hypertonic solution 3. 0.1 mM ouabain, whether in isotonic or hypertonic solution, does not influence the resting 24Na uptake, and does not decrease the 24Na uptake increasing effect of veratrine in isotonic media; however, in hypertonic solution it inhibits the 24Na uptake increasing effect. 4, 5 X 10(-8) M tetrodotoxin blocks completely the 24Na uptake enhancing effect of veratrine both in isotonic and in hypertonic Ringer's solution. 5. It is suggested that the sites of action of the 24Na uptake increasing effect of veratrine are the neural structures in muscle, in hypertonic media.

Animals↗
PubMed1976

Concentration dependence of the veratrine effect on inducing depolarization and membrane potential oscillation in skeletal muscle.

The concentration dependence of the effect of veratrine in inducing depolarization and membrane potential oscillation in the frog sartorius muscle has been studied. (1) On increasing the veratrine concentration from 0.025 to 1 mM, the latency period of the development of membrane potential oscillation and depolarization is proportionally shortened. (2) On changing the veratrine concentration from 0.025 to 1 mM, the magnitude of depolarization is raised logarithmically. (3) When the veratrine concentration reaches 0.05-0.1 mM, both the amplitude and the frequency of the membrane potential oscillation increase. On rising to 1 mM, a further increase in frequency to eight-fold occurs especially in the later phase of oscillation. At this concentration range, the amplitude of oscillation inversely proportional to the concentration of veratrine. (4) On increasing the veratrine concentration above 0.1 mM, the membrane potential oscillation ceases after a temporary rise of frequency. This inhibitory effect of veratrine is, however, reversible, and oscillations appear again, despite the absence of veratrine in Ringer's solution. This also proves the persistance of the veratrine effect.

Animals↗
PubMed1976

A two year trial of loxapine succinate in chronic psychotic patients.

Thirty-one chronic psychotic patients were treated with loxapine succinate, 20 for two years and eleven for one year, in order to evaluate its long-term efficacy and safety. Results presented here indicate that loxapine succinate is an effective treatment for chronic schizophrenia over a period of at least two years. Improvement, which occurred during the first six months of treatment (mostly during the first month), was maintained over the following year and a half. Unwanted effects were most frequent inthe early months of treatment and decreased as the two year trial progressed. No specifically long-term side effects were observed. The most frequent side effects were mild to moderate extrapyramidal signs. Blood pressure decreased and pulse rate increased, while remaining within normal limits, and returned to normal or near normal levels during the second year of treatment. Weight increased steadily during the two years and dropped markedly during the four week post-drug period. No drug-related abnormal laboratory findings were observed. It may be concluded that loxapine succinate is a safe and effective maintenance treatment for chronic schizophrenia.

Adult↗
PubMed1976

Psychotic exacerbations produced by neuroleptics.

Thirteen schizophrenic patients who developed abnormal psychotic behavior as an adverse reaction to a neuroleptic are described. A. Three patients showed a marked increase in the psychopathology during neuroleptic treatment. These episodes were treated by decreasing or discontinuing the neuroleptics. They did not respond to anticholinergic durgs nor did they respond to an increase in dosage, (another side effect previously reported and referred to here) indeed this treatment worsened the situation. B. Ten patients showed a mixed picture of catatonic excitement or inhibition on neuroleptics and several developed hallucinatory episodes. All of these exacerbations were terminated by anticholinergic injections. Other more familiar CNS abnormalities produced by neuroleptics are briefly discussed.

Acute Disease↗
PubMed1975

The physostigmine depolarization potentiating effect of salicylate in frog skeletal muscle.

1) The frog's sartorius muscle was depolarized depending on the degree of concentration 2--4 times more intensely by physostigmine salicylate than by physostigmine sulphate. 2) In normal Ringer's solution, 1 mM physostigmine salicylate decreased the sensitivity of the membrane to potassium depolarization by about 90%. Under similar experimental conditions, physostigmine sulphate and Na salicylate, respectively, decrease the sensitivity of the membrane to potassium depolarization by about 30%. 3) The difference manifested in the depolarizing effect of salicylate and other physostigmine salts (chloride, sulphate, phosphate, formiate, acetate, monochloracetate, benzoate and para-oxy-benzoate) is expressed already at 1 mM concentration (about 10-fold), if the muscle had been equilibrated in chloride-free glucuronate or sulphate milieu. 4) The depolarization develops slowly. It takes 30--60 minutes for the new steady state to develop even in the superficial sartorius fibres. If depolarization has reached its maximum on an average 100 mV, the membrane potential remains unchanged for hours. 5) Depolarization ensues at an unchanged degree in the presence of Na-free (choline) Ringer as well as in the presence of 2X10(-8) g/ml tetrodotoxin; therefore, it is not a Na-dependent process. 6) Under the influence of 1 mM physostigmine salicylate the membrane's resistance to the inward potassium current increased about twofold, while the increase was only 15% to the outward potassium current. It is assumed that the salicylate anion is characteristically capable of potentiating the decreasing effect of physostigmine on potassium permeability, though the role of the metabolic effect of salicylate cannot be excluded.

Animals↗