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Biomedical subjects

J Bajgar

Publications and source records attributed to J Bajgar.

At least 91 records · Page 5Linked to original sources
PubMed1978

Actions of O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate and some pyridine aldoximes on isolated guinea-pigs heart atria.

1. The effects of acetylcholine and methylfurmetide on isolated guinea-pigs heart atria in the presence or absence of O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate (EDMM) were investigated. The influence of three cholinesterase reactivators on the heart atria pretreated with EDMM has been studied. 2. In the presence of EDMM, the negative inotropic effect of acetylcholine on the isolated heart atria was not significantly increased. This effect of methylfurmetide on heart atria was significantly decreased in the presence of EDMM. 3. EDMM alone caused negative inotropic and negative chronotropic effects depending on its concentration. These pharmacological effects were accompanied with inhibition of acetylcholinesterase activity in the heart muscle. 4. Addition of cholinesterase reactivators normalized the inotropic response of the isolated guinea-pig heart atria altered by EDMM and also increased the acetylcholinesterase activity in the heart.

Acetylcholine↗
PubMed1978

Toxicities and the rates of penetration of O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate into the blood following different routes of intoxication.

Toxicities of O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate were determined by i. v. (17.0 microgram/kg), i.m. (23.6 microgram/kg), i. p. (54.5 microgram/kg) and p. o. (121.9 microgram/kg) administration to female rats. Following intoxication with this compound (42 microgram/kg) at these routes of administration, acetylcholinesterase activity in the blood was continuously monitored and half-times of inhibition in vivo were determined. It appears from a comparison of inhibitions in vivo and in vitro that only a part of the dose administered is effective to inhibit acetylcholinesterase in the blood vessel.

Acetylcholinesterase↗
PubMed1978

Detoxication of phosphonothioates and phosphonofluoridates in the rat.

0-isopropylmethyl phosphonofluoridate and 0-ethyl-S-(2-dimethylaminoethyl) methylphosphonothioate were i.m. administered in doses of 2 x LD50 to female rats and the blood acetylcholinesterase was continuously monitored using the automatic colorimeter Auto Analyzer. This activity rapidly decreased after the injection of the two organophosphates studied. If the blood flow in the leg muscles was stopped by compression and reopened by relaxation at different time intervals, acetylcholinesterase activity was either unaffected (detoxication present) or decreased (detoxication absent). It was observed that phosphonofluoridate was detoxified; on the other hand, phosphonothioate was not detoxified in the rat organism.

Acetylcholinesterase↗
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↗
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↗