Biomedical subjects
Publications and source records attributed to J Patocka.
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Acetylcholinesterase activity in rat blood was continuously monitored following O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate intoxication (p.o.) alone and in combination with atropine and the reactivators trimedoxime, obidoxime and methoxime. Decrease of acetylcholinesterase activity was not influenced by atropine alone but following treatment with a combination of atropine with the reactivators mentioned, an increase (reactivation) of the blood enzyme was demonstrated. This increase was highest for the combination atropine-trimedoxime and the lowest for the combination atropine-obidoxime.
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In vivo inhibition of blood acetylcholinesterase activity by 9-amino-1, 2, 3, 4-tetrahydroacridine, its 7-methoxy derivative and physostigmine was studied in rats. Changes of enzyme activity in the blood were continually registered using an automatic colorimeter Auto Analyzer system. The dependence of % enzyme inhibition upon time in semilogarithmic transformation was characterized by a two phase curve. The first phase reflected the increase in the concentration of inhibitors in the blood during their resorption; this was followed by a slow second phase of inhibition. The inhibitory effect decreased in the order: physostigmine greater than tacrine greater than 7-methoxytacrine. The relationship between the anticholinesterase and antipsychotomimetic action of the examined substances is discussed.
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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.
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.
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.