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Biomedical subjects

J Patocka

Publications and source records attributed to J Patocka.

At least 73 records · Page 4Linked to original sources
PubMed1977

Continual determination of acetylcholinesterase inhibition following organophosphate poisoning using an auto analyzer.

A modification for continual monitoring of the blood acetylcholinesterase activity in the rat on an auto analyzer system was described. With using this technique, inhibition of the enzyme in vitro with O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate was determined. Bimolecular rate constant and I50 values were 1.66-10(6) M-1-min-1 and 1.4-10(-8)M, respectively. Rats treated i.m. with 0.043 mg/kg of this compound showed fast and rapid inhibition of the blood acetylcholinesterase after intoxication. The bimolecular rate constant of inhibition in vivo, calculated analogously as that in vitro was 1.37-10(6) M-1-min-1. On the presumption that both rates of inhibition (in vitro and in vivo) are identical, the concentration of organophosphate producing inhibition effect in vivo was 82% of the dose administered.

Acetylcholinesterase↗
PubMed1976

Anticholinesterase action of 3-diethylaminophenyl-N-methyl-carbamate methiodide in vitro and in vivo.

The inhibitory effect of 3-diethylaminophenyl-N-methylcarbamate methiodide on rat brain acetylcholinesterase and horse plasma butyrylcholinesterase was studied in vitro. This quaternary carbamate is a more potent inhibitor of acetylcholinesterase than butyrylcholinesterase. Complete inhibition of acetylcholinesterase may be achieved without any inhibition of butyrylcholinesterase, i.e. that 3-diethylaminophenyl-N-methylcarbamate methiodide is a selective inhibitor of acetylcholinesterase. The inhibitory effect of different doses of this compound on plasma and liver butyrylcholinesterase and erythrocyte, brain, heart and diaphragm acetylcholinesterase of the rat was studied in vivo. With increasing doses of carbamate the inhibition of the enzymes in the plasma, erythrocytes, liver, heart, and diaphragm increased while the brain acetylcholinesterase was unaffected. The toxic action of carbamate studied was preferably due to acetylcholin esterase inhibition in the peripheral nervous system and this compound cannot penetrate the blood-brain barrier.

Animals↗
PubMed1976

The effects of some cholinesterase reactivators on contractility of the isolated guinea-pig heart atria.

The effect of eight monoquaternary and bisquaternary pyridine aldoxime cholinesterase reactivators was tested on isolated guinea-pig heart atria. 2. Acetylcholine and methylfurthretonium in concentrations ranging from 10(-7) M to 10(-5) M have negative inotropic effects in the electrically stimulated atria and negative chronotropic effects in the spontaneously beating atria. 3. In the presence of higher concentration of cholinesterase reactivators alone, the parameters of heart muscle contractility are significantly altered. 4. Cumulative dose-response curves of methylfurthretonium in the presence of reactivators in the range of concentrations from 10(-5) M to 10(-3) M are shifted parallelly to higher concentrations of the agonist.

Acetylcholine↗
PubMed1975

Antidotal therapy and changes of acetylcholinesterase activity following isopropyl methylphosphonofluoridate intoxication in mice.

The antidotal action of atropine with trimedoxime, obidoxime or methoxime against isopropyl methylphosphonofluoridate intoxication in mice was studied. The best antidotal effect was demonstrated for the combination of atropine and methoxime (tested as therapeutic index or D50 index). The effect of atropine (constant dose) and methoxime (different doses) on acetylcholinesterase (AChE) activity in four parts of the mouse brain following isopropyl methylphosphonofluoridate intoxication was described. The therapeutic effect could be improved by increasing dose of methoxime. AChE activity in the pontomedullar area was increased on increasing the dose of methoxime (p less than 0.005). A correlation between residual AChE activity in the pontomedullar part of the mouse brain and mortality was demonstrated.

Acetylcholinesterase↗