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Biomedical subjects

M F Kamynina

Publications and source records attributed to M F Kamynina.

13 recordsLinked to original sources

[Mechanism of the species characteristics of the sensitivity of monkeys and dogs to the emetic action of various pharmacological agents].

Monkey and dog sensitivity to the emetics that stimulate catecholamino- and serotoninoreactive structures of the chemoreceptor trigger zone (CTZ) of the vomiting center has been studied. It has been found that the monkeys are sensitive to the vomiting effect of serotonin agonists, while the dogs to the stimulants of the dopamino- and adrenoreceptors of the CTZ. At the same time both the monkeys and dogs are equally sensitive to the emetic action of sodium salicylate. The latter's effect has been shown to be realized via the serotoninergic structures of the CTZ in the monkeys, and via the adrenergic structures in the dogs. It is suggested that specific features of the monkey and dog responses to administration of central emetics are determined by the differences in the neurochemical structure of the CTZ, particularly by the prevalence of the serotonin- or catecholamine-containing neurons.

Animals↗

[Effect of dimetpramid and metoclopramide on the rate of catecholamine turnover in the subcortical-stem structures of the rat brain].

Dimetpramide, a new antiemetic drug (manufactured in the USSR) from the group of substituted benzamides, produced, due to blockade of catecholaminergic receptors, an increase in dopamine and noradrenaline turnover rates in the subcortical-brainstem regions responsible for the behavioural activity when administered at considerably higher doses than those of metoclopramide, a conventional drug of similar type. It is suggested that the probability of the occurrence of undesirable side effects of dimetpramide in clinical practice (extrapyramidal and sedative effects) would be much less than with metoclopramide.

Animals↗

[The effect of irradiation on dopamine level and metabolism in the rat brain].

In experiments on rats it was shown that after 20 Gy irradiation dopamine and homovanilic acid content increases in the caudate nucleus and limbic structures of the forebrain: dopamine disappears more readily when its biosynthesis is blocked. The rate of the mediator degradation in the brain increases by 1.5-2 times, and the rate of the synthesis, by 3-5 times at early times after irradiation.

Animals↗

[Modifying effect of radiation on phenamine hyperactivity].

Irradiation of rats with a dose of 20 Gy exerts a pronounced inhibitory action on the stimulation by phenamine of their behaviour activity. Since the ability of the preparation to increase the synthesis and release (degradation) of dopamine and norepinephrine does not change the effect of radiation it is suggested that under the action of radiation the sensitivity of catecholaminergic ceptors to the effect of the corresponding neuromediators decreases.

Amphetamine↗

[Antiemetic activity of dimetpramid].

It has been shown that dimethpramide, a new Soviet-made antiemetic belonging to the group of substituted benzamides, effectively prevents the emetic action of L-DOPA and apomorphine in dogs (the ED50 is 0.04 and 0.12 mg/kg, respectively). When given in doses of 10-25 mg/kg dimethpramide suppresses vomiting induced by adrenaline, histamine, strophanthine, sodium salicylate, and copper sulfate. The drug exerts a selective dopamine-blocking action on the receptors of the triggering zone of the vomiting center without producing any substantial action on the dopaminergic brain systems that regulate behavioral activity.

Animals↗

[Mechanism of emetic action of adrenaline and histamine in the dog].

It has been established in dog experiments that phentolamine prevents the emetic action of adrenaline whereas diphenhydramine the emetic effect of histamine. Both the drugs in the doses studied do not produce any effect on vomiting induced by L-DOPA. The dopamine blockers, etaperazine, haloperidol and metoclopramide given in the doses suppressing the emetic action of L-DOPA do not prevent the adrenaline- and histamine-induced vomiting. It is assumed that the emetic action of adrenaline is effected in dogs via alpha-adrenoreceptors, whereas the histamine-induced vomiting via H1-histamine receptors of the trigger zone of the vomiting center.

Animals↗

[Influence of catecholaminergic agents on the convulsant effect of corasol in rats].

It has been shown in experiments on rats that preinjection into the animals of amphetamine, isoprenaline hydrochloride, clonidine and phentolamine activating adrenergic transmission increases the resistance to the convulsant action of corasole. Disulfiram and guanethidine that decrease the content of noradrenaline in the body facilitate the development of corasole convulsions. The agents that change functional activity of the dopaminergic synapses (L-DOPA, alpha-methyldopa, apomorphine, perphenazine hydrochloride) exert no substantial effect on the convulsant effect of corasole. It is suggested that alpha- and beta-adrenergic structures participate in the mechanisms of catecholaminergic regulation of convulsant activity.

Animals↗

[Prostaglandins--their role in the mechanisms of the development of the primary reaction to radiation syndrome].

In experiments with dogs and rats it has been shown that early after high doses of irradiation, the content of prostaglandins in the blood plasma increases, whereas in the intestinal tissues it decreases. The inhibitors of prostaglandins synthesis indomethacin and voltaren hinder the development of early digestive disturbances, normalize the intestine absorptive and propulsive functions and make post-irradiation hypokinesia less pronounced. Possible mechanisms of the prostaglandins involvement in the genesis of prodromal radiation syndrome are discussed.

Animals↗