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J Patocka

Publications and source records attributed to J Patocka.

At least 37 records · Page 2Linked to original sources
PubMed1993

[Treatment of tardive dyskinesias with 7-methoxytacrine. I].

The 7-metoxytacrine (7-MEOTA) is an original Czech cholinergic agent synthetized in the labs of the Military Medical Academy in Hradec Králové. The treatment of tardive dyskinesias is one of the possible indications of the use of 7-MEOTA in clinical practice. The authors have summed up their experience from the first phase of clinical tests with 7-MEOTA in psychiatrical patients suffering from tardive dyskinesias in long-termed administration of cholinergic agents. The clinical efficiency and tolerance of 7-MEOTA have been evaluated after a single administration of 100 mg of 7-MEOTA per os in 19 patients. A reduction of dyskinesias was observed as early as 4 h following the testing dose. In 5 patients, viz. in 26% a reduction of dyskinesias was observed of more than 50% of the original value of the total score of the testing scale AIMS. Except for a slight decrease of the blood pressure and a mild somnolence in 3 patients no other undesirable effects have been observed. In some patients a slight euphorization effect of 7-MEOTA has been found.

Adult↗
PubMed1993

[Treatment of tardive dyskinesias with 7-methoxycrine. II].

In an open clinical study the authors have verified the effectivity and tolerance of 7-metoxytacrine cholinergic agent (7-MEOTA) in a total consisting of 14 patients with schizophrenic or schizoaffective psychoses suffering from tardive dyskinesias in long-termed treatment with neuroleptics. In the whole group consisting of 14 patients the seven days' administration of the experimental preparation in a dose of 100-150 mg pro die was evaluated. The 7-MEOTA preparation was administered to 7 patients for 2 weeks. In the seven and fourteen days' administration a favourable effect of 7-MEOTA on tardive dyskinesias was observed. A fast onset of the efficiency as early as in the first days of the treatment was recorded. In final evaluation a minimal reduction of 50% of the intensity of the dyskinesias (using the AIMS scale) in 29% of the patients treated for a fortnight was found. The 7-MEOTA preparation was well tolerated, no undesirable marked side effects being observed. A transient increase of ALT was found in 1 patient only in the 2nd week of the treatment. In experimental treatment the maintenance neuroleptical therapy was not discontinued. An improvement of the dyskinesias overlasted in some patients as long as 2 month g after the discontinuation of the administration of 7-MEOTA preparation.

Adult↗
PubMed1992

Acute toxicities of 2-dialkylaminoalkyl-(dialkylamido)-fluoro-phosphates.

Toxicities expressed as LD50 values of 2-dialkylaminoalkyl-(dialkylamido)-fluorophosphates for rats and mice (i.m. administration) were determined. Rats were more sensitive to these compounds than mice: LD50 values varied from 17 (rats) to 1222 (mice) micrograms/kg. LD50 values at different routes of administration (i.v., i.m., s.c., p.o. and p.c.) for one derivative of this group, 2-dimethylaminoethyl-(dimethylamido)-fluorophosphate, were determined. Depending on the route of administration, LD50 values varied from 11 (i.v.) to 190 (p.o.) micrograms/kg for rats and from 27.6 (i.v.) to 222 (p.o.) micrograms/kg for mice, respectively. Percutaneous toxicity in rats only (LD50 = 1366 micrograms/kg) was determined.

Animals↗
PubMed1992

2-Dialkylaminoalkyl-(dialkylamido)-fluorophosphates: acute toxicities.

Toxicities expressed as LD50 values of 2-dialkylaminoalkyl-(dialkylamid) o-fluorophophates for rats and mice (i. m. administration) were determined. Rats were more sensitive to these compounds than mice: LD50 values varied from 17 to 261 micrograms/kg for rats and from 30.5 to 1222 micrograms/kg for mice, respectively. Different routes of administration in one derivative of this group substituted by methyl groups only were compared. The highest toxicity (lowest LD50 value) in intravenous administration (11 micrograms/kg) and the lowest one in percutaneous (1366 micrograms/kg) were found.

Animals↗
PubMed1992

[Present trends in the development of drugs within the cholinesterase inhibitor group as therapeutic agents for Alzheimer's disease].

With prolongation of human age rises also the incidence of senile dementia, inclusive dementia of Alzheimer's type (DAT). At the same time the authors present views in the aetiology of this illness, the role of cholinergic mechanisms of the development dementia and they mention DAT treatment strategy focusing attention on a group of drugs-cholinesterase inhibitors.

Alzheimer Disease↗
PubMed1991

Efficacy of various pretreatment and therapy regimens against soman lethality in mice.

The efficacy of a number of drug pretreatment combinations in protecting mice against lethal effects of soman was determined. Pyridostigmine peroral pretreatment followed by intramuscular postpoisoning therapy with atropine, obidoxime and/or trimedoxime, and diazepam protected mice against the lethal action of soman. Combination of pyridostigmine with trihexyphenidyl, benactyzine and bis-(4-hydroxyiminomethyl) pyridinium-methane dichloride improved prophylactic action even further.

Animals↗
PubMed1991

[Biotransformation of the anticholinesterase agent, 9-amino-7-methoxy-1,2,3,4-tetrahydroacridine].

Biotransformation of the anticholinesterasic agent 9-amino-7-methoxy-1,2,3,4-tetrahydroacridine was studied in the laboratory rat. In the animal urine, the main identified metabolites were 9-amino-7-hydroxy-1,2,3,4-tetrahydroacridine and its conjugate with glucuronic acid, or sulfuric acid, as well as 9-amino-1-hydroxy-7-methoxy-1,2,3,4-tetrahydroacridine and 9-amino-2-hydroxy-7-methoxy-1,2,3,4-tetrahydroacridine. A part of the drug was excreted in an unchanged form.

Animals↗
PubMed1989

Effect of pyridostigmine and syntostigmine pretreatment on the inhibition of acetylcholinesterases by o-pinacolyl-methylphosphonofluoridate. In vitro experiments with rat tissues.

The inhibition kinetics of O-pinacolyl-methylphosphonofluoridate and two carbamates (pyridostigmine and syntostigmine) on the acetylcholinesterase from rat erythrocytes, brain and diaphragm have been studied in vitro. The affinity of O-pinacolyl-methylphosphonofluoridate to carbamates pretreated acetylcholinesterase was tested. In vitro addition of pyridostigmine and/or syntostigmine to acetylcholinesterase prior to the organophosphate provided a weak protection against acetylcholinesterase inhibition by this potent organo-phosphorous inhibitor.

Animals↗
PubMed1987

Inhibition of the butyrylcholinesterase by ethidium bromide.

The effect of ethidium bromide (3,8-diamino-5-ethyl-6-phenyl-phenanthridinium bromide) on the activity of purified horse serum butyrylcholinesterase in vitro has been studied. Ethidium bromide is a middle reversible inhibitor with complex mixed competitive-noncompetitive inhibition kinetics. The inhibitor is bound to the anionic site of the enzyme surface.

Animals↗
PubMed1987

Protective effect of bis-pyridinium compounds on the rat brain acetylcholinesterase inhibition by carbamate in vitro.

The inhibition of the rat brain acetylcholinesterase by quaternary bis-pyridinium compounds and the protection against acetylcholinesterase inhibition by 3-diethyl-aminophenyl-N-methylcarbamate methiodide was studied with three bis-pyridinium compounds. These compounds have two pyridinium rings connected by a dimethylether link and alkyl groups in position 4 of both pyridinium rings. Toxogonin was used as a reference compound. Bis-pyridinium compounds studied are weak reversible inhibitors of acetylcholinesterase (I50 from 10(-4) to 10(-3) M) and exert also the ability to protect acetylcholinesterase against inhibition by 3-diethyl-aminophenyl-N-methylcarbamate methiodide in vitro at a concentration of 0.1 mM. Negligible protection was obtained with Toxogonin.

Animals↗