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Biomedical subjects

Z Kleinrok

Publications and source records attributed to Z Kleinrok.

At least 235 records · Page 13Linked to original sources
PubMed1978

Biological properties and clinical application of propolis. X. Preliminary pharmacological evaluation of ethanol extract of propolis (EEP).

A study consisting of an examination of the acute toxicity of ethanol extract of propolis (EEP) in mice, its effect on spontaneous movement in mice and rats, its analgesic properties and its influence on body temperature in mice was conducted. Also examined was the activity of EEP on animals under the influence of narcotics and spontaneous movement under the influence of amphetamine, its effects on blood pressure and respiration in rats. The results of these examinations indicate that EEP injected i.p. has a weak general effect on the experimental animals.

Amphetamine↗
PubMed1977

Clonidine-induced locomotor hyperactivity in rats. The role of central postsynaptic alpha-adrenoceptors.

The alpha-adrenergic agonist, clonidine, causes sedation in normal rats. The present study demonstrates that clonidine evokes strong locomotor stimulation in rats pretreated with 6-hydroxydopamine plus reserpine. Similar, but less intensive hyperactivity is observed in rats given clonidine after combined pretreatment with 6-hydroxydopamine plus p-chlorophenylalanine plus alpha-methyl-p-tyrosine, or with reserpine plus low doses of yohimbine. The aplha-adrenolytic drugs, phenoxybenzamine, phentolamine and aceperone, as well as high doses of yohimbine, antagonise the clonidine-induced locomotor stimulation; in contrast, the dopamine receptor blocking agents, pimozide and spiroperiodol, exert no antagonistic effect. The results indicate that in the brain of normal animals, clonidine predominantly activates presynaptic alpha-adrenoceptors on noradrenergic neurones and thereby induces sedation. After destruction of the noradrenergic fibres by 6-hydroxydopamine plus reserpine, activation of postsynaptic alpha-adrenoceptors prevails so that hyperactivity results.

Adrenergic Agents↗
PubMed1977

The influence of dfp, atropine and toxogonine on tryptophan pyrolase activity in mouse liver.

It was found that fluorostigmine (DFP) in doses 0-4 mg/kg i.p. reduced significantly tryptophan pyrolase activity in mouse liver homogenates.se liver homogenates 120 and 180 min after the administration of the drug. On the other hand, fluorostigmine administered in doses 0-8 mg/kg i.p. increases the activity of the enzyme studied at 30 and 60 min after the injection. DFP (0.4 mg/kg i.p.) given in combination with atropine (10 mg/kg i.p.) causes a significant increase in enzyme activity determined 30, 60, 120 and 180 min after the administration of the drug. Toxogonine (in doses 5 mg/kg s.c.) given together with DFP (0.4 mg/kg i.p.) intensifies the activity of tryplophan pyrolase at 180 min after their administration. Simultaneous treatment with toxogonine (5 mg/kg s.c.), atropine (10 mg/kg i.p.) and DFP (0.4 MG/KG I.P.) reduced significantly the activity of the enzyme studied at all time of determination. Moreover, the experiment in vitro showed that DFP in concentrations of 4x10(-9) M; 8X10(-9) M; 1.6X10(-8) M and 3.2x10(-8) M increased tryptophan pyrolase activity in mouse liver homogenates.

Animals↗
PubMed1976

A comparison of the central actions of prostaglandins A1, E1, E2, F1alpha, and F2alpha in the rat. II. The effect of intraventricular prostaglandins on the action of some drugs and on the level and turnover of biogenic amines in the rat brain.

Prostaglandins (PGs) injected into the right lateral brain ventricle (i.v.c.) of the rat increased the sleeping time induced by hexobarbital, chloral hydrate, and ethanol. PGE1 and PGE2 intensified chlorpromazine-induced catalepsy, inhibited amphetamine hyperactivity, and significantly depressed the amphetamine-induced stereotypy. NA concentrations were decreased by PGE1 and PGE2 and were increased by PGF2alpha. PGF2alpha increased both 5-HT and 5-HIAA levels in rat brain. "Total" ACh concentrations were increased by PGF1alpha and PGF2alpha. PGE1, PGE2, and PGF2alpha enhanced the turnover of NA, DA, and 5-HT. PGE2 counteracted the decreased activity induced by alpha-MT and abolished the hypothermic action of alpha-MT. PGF2alpha had little effect on the activity of PCPA pretreated rats, whereas the higher doses of PGF2alpha increased body temperature in these animals.

Acetylcholine↗
PubMed1976

Potential acetylcholinesterase reactivators: oxime and amidoxime derivatives.

Out of 12 oximes and amidoximes (3 of which were new to the literature) the following showed a distinct antilethal effect in DFP poisoning: RA14 (1-methylbenzimidazole-2-aldoxime methiodide), RA14 (pyridine-4-aldoxime dodecyl bromide), and RA24 (pyridine-2-aldoxime dodecyl bromide). These compounds also reactivated acetylcholinesterase (AChE) in vitro, but had no effect on this enzyme in vivo. Moreover, addition of the dodecyl chain to pyridinealdoxtimes, or in a less degree replacement of the pyridine ring with benzimidazole in aldoximes, distinctly increased acute toxicity and lipophilicity when compared with the parent pyridine compounds, along with protective action in DFP poisoning.

Acetylcholinesterase↗