Search PubMed⌕ Search

Biomedical subjects

V Dolezal

Publications and source records attributed to V Dolezal.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Hyperbaric oxygen therapy].

Oxygen inhalation in a chamber at the pressure exceeded 0.2 MPa produces some positive effects, that are explored for therapeutic purposes at about 30 years. Oxygen increases bactericidal capacity of leukocytes, reduces tissue edema, protects intracellular ATP, maintain tissue oxygenation even in the absence of hemoglobin. Stimulates fibroblast replication, increases collagen production, stimulates arborisation of capillaries into ischemic tissue, protects from lipid peroxidation. These properties of oxygen are exploit in acute, life threatened conditions and in various chronic ischemias. Hyperbaric oxygen therapy as an adjuvant together with conservative and invasive therapy methods helps to decrease morbidity, work incapability, invalidisation and mortality in oclusive and inflammatory arteriities, diabetic gangrene and other forms of clinical leg ischemia. The use of hyperbaric oxygenation will become increasingly common as more hyperbaric facilities are established.

Humans↗
PubMed1995

Differences of the electrical and nicotinic receptor stimulation-evoked liberation of norepinephrine from chicken sympathetic neurons in culture: possible involvement of different pools of the transmitter.

We studied the release of [3H]norepinephrine from chicken sympathetic neurons in culture evoked by nicotinic and electrical stimulation with an intention to establish functional identity or nonidentity of the two stimuli in investigations of neurotransmitter release. Nicotinic stimulation evoked extracellular calcium dependent release of [3H]norepinephrine and the rise of intracellular calcium concentration. The release was completely blocked by nicotinic antagonists hexamethonium (100 mumol/l) and mecamylamine (10 mumol/l), and decreased by tetrodotoxin (0.3 mumol/l) and omega-conotoxin (0.1 mumol/l) to 17% and 27%, resp. The intracellular calcium response was decreased by nicotinic antagonists and tetrodotoxin, but not changed by omega-conotoxin. The electrical stimulation-evoked release was blocked by both tetrodotoxin and omega-conotoxin, and decreased by previous electrical, but not nicotinic, stimulation. The differential sensitivity to omega-conotoxin and tetrodotoxin,and the inability of nicotinic stimulation to decrease the liberation by following electrical stimulation may suggest the mobilization of different pools of the transmitter.

Action Potentials↗
PubMed1995

Presynaptic nicotinic receptors stimulate increases in intraterminal calcium of chick sympathetic neurons in culture.

Stimulation of chick sympathetic neurons in culture by the cholinergic agonists acetylcholine, nicotine, and 1,1-dimethyl-4-phenylpiperazinium (all at 10-1,000 mumol/L) induced concentration-dependent increases of free calcium levels measured by fura 2 fluorescence in neuronal processes. The response evoked by acetylcholine had both nicotinic and muscarinic components, whereas that induced by 1,1-dimethyl-4-phenylpiperazinium was purely nicotinic. Tetrodotoxin (0.3 mumol/L) blocked completely the increase of intraterminal free calcium level evoked by electrical stimulation. On the other hand, stimulation with 1,1-dimethyl-4-phenylpiperazinium still evoked 20-25% of the control response in the presence of tetrodotoxin. The concentration-response relationship of 1,1-dimethyl-4-phenylpiperazinium stimulation did not differ in the absence and in the presence of tetrodotoxin. The nicotinic antagonists d-tubocurarine (10 mumol/L) and mecamylamine (10 mumol/L), but not alpha-bungarotoxin (125 nmol/L), prevented the increase of intraterminal free calcium level evoked by 1,1-dimethyl-4-phenylpiperazinium (100 mumol/L) in the presence of tetrodotoxin. These observations indicate the presence of nicotinic receptors on neuronal processes that increase the intraterminal concentration of free calcium and probably modulate transmitter release. Their pharmacological properties are similar to those of nicotinic receptors located on neuronal cell bodies.

Acetylcholine↗
PubMed1994

Presynaptic alpha 2-adrenoceptors inhibit calcium influx in terminals of chicken sympathetic neurons and noradrenaline release evoked by nicotinic stimulation.

The changes of intracellular calcium concentration evoked by stimulation of nicotinic receptors and its modulation by alpha 2-adrenoceptors were investigated in chicken sympathetic neurons grown in culture. Stimulation of nicotinic receptors increased the intracellular calcium both in the area of cell bodies and processes. In normal extracellular calcium (1.3 mmol/l), the specific alpha 2-adrenoreceptor agonist UK 14,304 (10 mumol/l) diminished the response in cell bodies but not in processes. The same treatment in medium with reduced calcium (0.13 mmol/l) resulted in the decrease of the response evoked by nicotinic stimulation in the area of processes but not in the cell bodies. The effect of UK 14,304 on evoked noradrenaline release paralleled its influence on intracellular calcium in processes. These data indicate that nicotine stimulation-induced influx of calcium is inhibited by alpha 2-adrenoceptor stimulation both in cell bodies and in processes. It is concluded that the nicotinic stimulation-evoked release of noradrenaline is triggered by influx of calcium through alpha 2-adrenoreceptor sensitive as well as insensitive pathways.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1993

Presynaptic muscarinic receptors and the release of acetylcholine from cerebrocortical prisms: roles of Ca2+ and K+ concentrations.

The mechanism by which presynaptic muscarinic autoreceptors inhibit the release of acetylcholine (ACh) from cerebrocortical cholinergic fibres has not been clarified. To test the view that muscarinic autoreceptors act by decreasing Ca2+ influx, we performed experiments in which rat cerebrocortical prisms were preloaded with (14C)choline, washed, depolarized with 14-65 mM K+ in the absence of Ca2+ and then exposed (still under depolarization) to various concentrations of Ca2+ to evoke the release of (14C)ACh. The muscarinic agonist, oxotremorine, used at a 100 microM concentration, inhibited the release of (14C)ACh by 59-86% in experiments with 14 and 26.5 mM K+ but had no significant effect at 65.5 mM K+. No systematic changes in the inhibitory effects of oxotremorine could be found at any of the K+ concentrations used when the concentration of Ca2+ was varied in the range of 0.25-4.0 mM. At 2 mM Ca2+ and K+ concentrations above 14 mM, the inhibitory effect of oxotremorine was inversely related to the concentration of K+. The inhibitory effect of oxotremorine on (14C)ACh release was not blocked by 100 microM 4-amino-pyridine. The fact that the inhibitory effect of oxotremorine could not be overcome by an increase in the concentration of Ca2+ suggests that, under the conditions used, a restriction of the influx of Ca2+ did not play a major role in the muscarinic inhibition of ACh release; rather, oxotremorine appeared to act by decreasing membrane depolarization.2+ of the Ca(2+)-voltage hypothesis of neurotransmitter release, supposing

Acetylcholine↗
PubMed1993

Effect of N,N'-dicyclohexylcarbodiimide on compartmentation and release of newly synthesized and preformed acetylcholine in Torpedo synaptosomes.

Using isolated cholinergic synaptosomes prepared from Torpedo electric organ, we studied the effects of N,N'-dicyclohexylcarbodiimide (DCCD) on acetylcholine (ACh) synthesis, compartmentation, and release after stimulation. Whereas ACh synthesis was unchanged, ACh compartmentation inside synaptosomes was affected by the presence of DCCD. In resting conditions, the uptake into the synaptic vesicle pool of newly synthesized ACh (i.e., [14C]ACh synthesized in the presence of the drug) was progressively and markedly inhibited as the duration of DCCD preincubation was increased, whereas compartmentation of endogenous ACh was unchanged in the presence of DCCD. After stimulation, the release of endogenous ACh from DCCD-treated synaptosomes was similar to that of control, in contrast to the release of [14C]ACh, which was markedly inhibited. This inhibition was observed whatever the conditions of stimulation used (gramicidin D, calcium ionophore A23187, or KCl depolarization). The study of the compartmentation of [14C]ACh during stimulation revealed a transfer of highly labeled ACh from the free to the bound ACh compartment in the presence of DCCD, suggesting the existence of several ACh subcompartments within the free and bound ACh pools. The present results are discussed in comparison with the previously reported effects of vesamicol (AH5183) on ACh compartmentation and release.

Acetylcholine↗
PubMed1992

Activation of dopamine D1 receptors does not affect D2 receptor-mediated inhibition of acetylcholine release in rabbit striatum.

The possible involvement of dopamine D1 receptors in the regulation of acetylcholine release in the rabbit caudate nucleus was investigated. Caudate slices, preincubated with [3H]choline, were superfused continuously and subjected to electrical field stimulation with only a single pulse. In agreement with the view that the release of acetylcholine evoked by a single electrical pulse is not influenced by endogenous transmitters, atropine and domperidone failed to increase the evoked release of [3H]acetylcholine, whereas oxotremorine and quinpirole caused a concentration-dependent inhibition of transmitter release. Neither the dopamine D1 receptor antagonist SCH 23390 nor the D1 agonist SKF 38393 in a concentration range of 0.01-1 mumol/l changed the evoked [3H]acetylcholine release. The inhibitory effect of the dopamine D2 receptor agonist quinpirole was virtually abolished in the presence of 0.1 mumol/l domperidone and diminished in the presence of 1 mumol/l SCH 23390. It remained unchanged in the presence of 1 mumol/l SKF 38393. It is concluded that the inhibition of acetylcholine release by dopamine is mediated exclusively via presynaptic dopamine D2 receptors and that the antagonistic effect of SCH 23390 on the inhibition of acetylcholine release by quinpirole is due to its interaction with dopamine D2 rather than D1 receptors located on cholinergic nerve terminals.

Acetylcholine↗
PubMed1992

Investigation of the mechanism of the effect of tacrine (tetrahydroaminoacridine) on the metabolism of acetylcholine and choline in brain cortical prisms.

The mechanism by which tacrine increases the content and synthesis of acetylcholine (ACh) in cerebrocortical prisms exposed to an irreversible inhibitor of cholinesterases and incubated under resting conditions (Dolezal and Tucek, 1991) is not known. As found in the present experiments, this effect of tacrine is only apparent if its application had been preceded by a period of preincubation, but the preincubation is ineffective if it occurs in the presence of hemicholinium-3. Apparently, choline or a choline-containing compound accumulates in the slices during the preincubation and is then utilized for the enhanced synthesis of ACh in the presence of tacrine. Tacrine did not induce a decrease in the amount of radiolabel that had been incorporated from choline into acid-insoluble compounds, which suggests that the choline which is used for the synthesis of additional ACh does not originate from choline lipids. However, tacrine was found to diminish the efflux of choline from prisms which had been preincubated with an increased concentration of choline in the medium, and from prisms incubated in the presence of hemicholinium-3. It also diminished the efflux of radioactive choline that had accumulated in the prisms during preincubation with a very low concentration of tacrine, when the prisms were subsequently incubated with 4-aminopyridine. It is proposed that the potency of tacrine to increase the content and synthesis of ACh in cerebrocortical prisms whose cholinesterases had been inhibited is due to its ability to diminish the efflux of endogenous choline from the nerve terminals.

4-Aminopyridine↗
PubMed1992

Effects of tetrodotoxin, Ca2+ absence, d-tubocurarine and vesamicol on spontaneous acetylcholine release from rat muscle.

1. Rat hemidiaphragms were incubated in a physiological low-K+ medium without stimulation and the amount of acetylcholine (ACh) released was measured radioenzymatically. Cholinesterases were inhibited by paraoxon. 2. In the presence of 1 microM tetrodotoxin (TTX), the amount of ACh released during a 2 h incubation was lowered by 40%. A similar decrease was observed in the absence of Ca2+ and in the presence of 10 microM-d-tubocurarine (dTC). The effects of TTX combined with Ca2+ removal, and of TTX combined with dTC were no greater than those of TTX, dTC or Ca2+ removal alone. TTX and dTC had no effect on the release of ACh from diaphragms 4 days after denervation. 3. The reduction of spontaneous ACh release observed in the presence of TTX or dTC or in the absence of Ca2+ is best interpreted on the assumption that about 40% of the ACh release was due to the impulse activity known to be generated in intramuscular motor nerve branches by the ACh which accumulates after the inhibition of cholinesterases. 4. In the presence of 1 and 10 microM vesamicol (AH5183, 2-(4-phenylpiperidino)-cyclohexanol), the release of ACh was also diminished by approximately 40%. Vesamicol did not augment the inhibition of release produced by TTX or by the omission of Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

[Air embolism].

Air embolism is a dramatic event which threatens the patient's life during invasive therapeutic and diagnostic procedures. Immediately after establishment of the diagnosis treatment in a hyperbaric chamber should be started. The prognosis depends to a certain extent on how quickly the patient is transferred into a hyperbaric chamber. Treatment with hyperbaric oxygen is based on fundamental physical and physiological principles of the action of compressed air and the supply of a large amount of oxygen in a dissolved form into the ischaemic tissue beyond the obstruction. Installation of hyperbaric chambers in hospitals would make successful and prompt treatment of all cases of embolism possible, as well as of some other diseases indicated for hyperbaric oxygen therapy.

Embolism, Air↗
PubMed1991

[Forced expiration and inspiration under hyperbaric conditions].

In 37 healthy men aged 23-53 years the ratio of one-second and forced vital capacity of the lungs during forced inspiration and expiration FIV1/FIVC and FEV1/FEVC was recorded, (i.e. 0.901 as compared with MPa) a significantly higher value of FIV1/FIVC than of FEV1/FEVC was recorded, (i.e. 0.901 as compared with 0.857, p less than 0.05), at pressure of 0.4 MPA the reverse occurred: variable FIV1/FIVC was substantially smaller than FEV1/FEVC (0.635 vs. 0.731, p less than 0.01). The authors express the view that this phenomenon could be explained by the theory which assumes that the expiratory muscles in healthy subjects do not display during forced expiration their maximum strength and only under hyperbaric conditions when the stream resistance of the airways rises their strength is fully used. On the other hand, the maximal strength of the inspiratory muscles is involved already during normal pressure and thus a significant increase cannot occur under conditions of overpressure.

Adult↗
PubMed1991

Positive and negative effects of tacrine (tetrahydroaminoacridine) and methoxytacrine on the metabolism of acetylcholine in brain cortical prisms incubated under "resting" conditions.

The effects of tacrine (1,2,3,4-tetrahydro-9-aminoacridine) and 7-methoxytacrine on the metabolism of acetylcholine were investigated in experiments on prisms of rat cerebral cortex incubated in vitro in low-potassium (3 mmol/L K+) media; cholinesterases were inactivated by paraoxon to avoid any action of tacrine and methoxytacrine via their inhibition. Under "resting" conditions, tacrine and methoxytacrine increased the synthesis of unlabeled acetylcholine in the prisms; at the same time, they inhibited the uptake of [14C]choline from the medium and the synthesis of [14C]acetylcholine. The concentration of free choline was not increased by tacrine or methoxytacrine in either the tissue or the medium. The contradiction between the increased synthesis of unlabeled and the diminished synthesis of labeled acetylcholine indicates that the utilization of intracellular choline (which is presumably mobilized from intracellular choline esters) for the synthesis of acetylcholine is increased by tacrine and methoxytacrine. This conclusion is supported by the observation that the inhibition of acetylcholine synthesis during incubation with hemicholinium-3 (an inhibitor of choline transport into cholinergic nerve terminals) was overcome when tacrine was present simultaneously with hemicholinium-3. When the prisms were preincubated with [14C]choline and incubated with tacrine or methoxytacrine only after this, the amount of [14C]acetylcholine recovered in the tissue plus the medium was higher at the end of incubation with tacrine or methoxytacrine than without them, again suggesting that the drugs were able to increase the utilization of intracellular [14C]choline or its esters for acetylcholine synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1991

Negative effects of tacrine (tetrahydroaminoacridine) and methoxytacrine on the metabolism of acetylcholine in brain slices incubated under conditions stimulating neurotransmitter release.

The effects of tacrine (1,2,3,4-tetrahydro-9-aminoacridine) and 7-methoxytacrine on the metabolism of brain acetylcholine were investigated in experiments in which acetylcholine turnover was stimulated by tissue depolarization or by 4-aminopyridine. Rat cerebrocortical prisms were preincubated under "resting" conditions (Krebs-Ringer buffer with 3 mmol/L K+ and with paraoxon to inhibit cholinesterases) and then incubated in the presence of tacrine or methoxytacrine and of 50 mmol/L K+. Both drugs diminished the amount of acetylcholine released by depolarization and the amount of acetylcholine synthesized during incubation; in experiments in which [14C]choline was present in the incubation medium simultaneously with tacrine or methoxytacrine, the drugs diminished the uptake of [14C]choline by the tissue and the amount of [14C]-acetylcholine synthesized and released into the medium. In these experiments, it was not possible to distinguish whether the inhibitory effects of tacrine and methoxytacrine were primarily on the process of acetylcholine synthesis (particularly on the uptake of choline), or whether the drugs also acted directly on the process of neurotransmitter release. In subsequent experiments the prisms were preincubated with [14C]choline and only then subjected to a short depolarization in the presence of hemicholinium-3 and tacrine or methoxytacrine. Both drugs severely inhibited the release of preformed [14C]acetylcholine and prevented the diminution of tissue [14C]acetylcholine stores. Methoxytacrine was also found to diminish the release of acetylcholine induced by 4-aminopyridine while increasing the content of acetylcholine in the tissue. Tacrine and methoxytacrine had no effect on the activity of choline acetyltransferase (EC 2.3.1.6).(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1991

Modulation of acetylcholine release from rat striatal slices: interaction between 4-aminopyridine and atropine.

The objective of these studies was to determine whether the muscarinic receptor-mediated autoregulation of the basal release of acetylcholine (ACh), like the modulation of evoked release, involves 4-aminopyridine (4-AP)-sensitive potassium channels. To accomplish this, striatal and hippocampal slices were incubated with 4-AP in the absence or presence of atropine, and the release of ACh was measured. 4-AP increased the release of ACh in a concentration-dependent manner; a maximal effect (280% of control release) was achieved in the presence of 100 microM. The maximal release of ACh from hippocampal slices was approximately 150% of control release and was achieved in the presence of a broad range of concentrations (33-333 microM 4-AP). Tetrodotoxin (1 microM) totally abolished the 4-AP-induced release of ACh from hippocampal slices, but only attenuated the 4-AP-induced release from striatal slices, i.e., in the presence of tetrodotoxin, the 4-AP-induced release of ACh from the latter was significantly greater than control release by 54%. Atropine (0.1 microM) increased significantly the basal release of ACh from striatal slices by 61%. When striatal slices were incubated with 4-AP in the presence of this maximally effective concentration of atropine, ACh release was significantly greater than release from slices incubated with either atropine or 4-AP alone, suggesting that atropine and 4-AP increase neurotransmitter release by independent mechanisms. Although oxotremorine did not alter either the 4-AP- or atropine-induced release of ACh, it prevented the potentiated response exhibited by slices incubated with both atropine and 4-AP.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1990

Effects of atropine on the release of newly synthesized acetylcholine from rat striatal slices at various concentrations of calcium ions.

The release of acetylcholine (ACh) from brain tissue is known to be inhibited by muscarinic autoreceptors on cholinergic nerve terminals but the mechanism of the inhibition is not understood. Atropine brings about an increase of ACh release by removing the inhibitory action of autoreceptors. We investigated whether the effect of atropine on the release of [14C]ACh newly synthesized during incubations from [U-14C] glucose depends on the concentration of Ca2+ in the medium. In rat striatal slices incubated in the presence of an inhibitor of cholinesterases and of 30 mmol/l K+, significant increases in the release of [14C]ACh elicited by atropine were only observed during incubations with very low concentrations of Ca2+. This finding supports the view that the activation of presynaptic muscarinic autoreceptors in the brain affects the release of ACh by reducing the availability of Ca2+ that is required for transmitter liberation.

Acetylcholine↗
PubMed1990

Muscarinic receptor blockade increases basal acetylcholine release from striatal slices.

The main objective of these studies was to determine whether the basal release of acetylcholine (ACh) from brain slices was subject to modulation by muscarinic receptor blockade. Incubation of striatal slices with the muscarinic antagonist atropine increased ACh release in a concentration-dependent manner with a maximal effect (1.4-1.8 times control release) achieved with 0.1 to 1.0 microM. In contrast, ACh release from hippocampal slices was unaltered by any concentration of atropine tested, indicating that the basal release of neurotransmitter from striatum, but not hippocampus, was subject to modulation by muscarinic receptor blockade. Incubation of striatal slices with 1 microM tetrodotoxin or removal of Ca++ from the medium decreased the basal release of ACh by 20% and abolished the atropine-induced release of ACh; neurotransmitter release from hippocampal slices was unaltered by tetrodotoxin. Thus, part of the basal release of ACh from striatal slices is a consequence of the intrinsic impulse activity of cholinergic neurons and it is this component of release that is atropine-sensitive. Oxotremorine was unable to antagonize the atropine-induced release of ACh, even with concentrations 100 times that of atropine, whereas pirenzepine increased ACh release and, like that of atropine, the effect of pirenzepine was sensitive to tetrodotoxin and resistant to oxotremorine. These results indicate that a component of basal ACh release from striatal slices is subject to modulation by a receptor that is sensitive to atropine and pirenzepine, but not to oxotremorine, suggesting that this site differs from the nerve terminal muscarinic autoreceptor.

Acetylcholine↗