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A V Rychko

Publications and source records attributed to A V Rychko.

8 recordsLinked to original sources
PubMed1977

[Effect of lithium chloride on the rat hypothalamus neurosecretory system].

Methods of quantitative cytochemical analysis were applied to the study of the reaction of the hypothalamohypophysial neurosecretory system (HHNS) to single and course administrations of lithium chloride (in doses of 200 mg/kg). Reaction of the HHNS proved to depend directly on the amount of lithium administered and was characteriaed by the activation of the synthesis and elemination of the neurosecretion with a single administration on the preparation, or depression of the hormonopoiesis in the hypothalamus and exhaustion of the neurosecretion stores in the neurohypophysis in its course application. During the restoration (7 to 30 days after stopping the drug administration) the state of the HHNS gradually approached the initial level. The authors came to the conclusion that the changes in the central mechanisms of the neuro-endocrine regulation at the hypothalamic level caused by lithium were significant in the pathogenesis of the side-action of its salts

Animals↗
PubMed1976

[Role of the kidneys in the pathogenesis of lithium poisoning].

Lithium intoxication was induced in rats by intraperitoneal administration of lithium chloride in a daily dose of 200 mg/kg (0.22 LD50) for 6 days. Polyuria connected with pathological changes in the epithelium of the convoluted tubules and depression of the antidiuretic hormone--acid mucopolysaccharides system in the area of the straight kidney tubules was observed on the 6th day of the experiments. Oligouria and death of some of the animals on the 7th experimental day was caused by severe lesions the kidney structure. Further observation (30 days) demonstrated that, along with the regeneration processes, there developed a marked sclerosing ofthe kidney tissue. A conclusion was drawn that severe lithium intoxication was associated with the development of acute renal insufficiency. Functional reserves of the kidneys after the cessation of lithium chloride administration remained lowered for a long period.

Acute Kidney Injury↗
PubMedDate not supplied

Effect of lithium chloride on the neurosecretory system of the rat hypothalamus.

The response of the hypothalamic-pituitary neurosecretory system (HPNS) of rats to a single and repeated injection (200 mg/kg each time) of lithium chloride was studied by quantitative cytochemical analysis. The response of the HPNS was found to depend directly on the dose of lithium given and to consist of activation of synthesis and liberation of neurosecretion after a single dose of LiCl or inhibition of hormone formation in the hypothalamus and exhaustion of the reserves of neurosecretion in the neurohypophysis after a course of injections. In the recovery period (7--30 days after stopping the course of injections of LiCl) the previous state of the HPNS was gradually restored.

Animals↗
PubMedDate not supplied

[Pathogenesis of lithium polyuria].

An attempt is made to elucidate the pathogenesis of polyuria arising consequent upon medication of affective states with lithium salts. Experiments conducted with 54 male-rats showed that changes in the neurosecretion of supraoptic nuclei of the hypothalamus and neurohypophysis that take place after a course-wise intraperitoneal administration in amounts of 200 mg/kg (2/9DL20) of lithium chloride per 24 hours for a duration of 6 days occur parallel with histochemical changes of renal acid muconpolysaccharides and they accord with the nature of diuresis disorders. By the 5th day of the experiment the compound perverts the antidiuretic effect of a single subcutaneous injection of pituitrin (10 U/kg). The authors infer therefrom that polyuria emerging after introduction of lithium salts is caused by a deranged synthesis and secretion of the diuretic hormone and also by the ability of lithium to mitigate the action of this hormone on the kidneys.

Animals↗
PubMedDate not supplied

[Effect of lithium hydroxybutyrate on several heart function indices].

DL50 of intraperitoneal lithium oxybutyrate administered to cats was found to amount to 724 mg/kg, while in doses of 13.5--360 mg/kg it increases the coronary blood flow volume in cats by 20.3--122.2 per cent, directly proportional to the dose. Lithium oxybutyrate prevents the chlorocalcium arrhythmia in rats and eliminates strophanthine-induced anemia in cats, surpassing an analogous effect of lithium chloride, potassium chloride, quinidine, novocainamide and isoptin. It raises the activity of the succinate dehydrogenase in the myocardium and weakens the ability of calcium chloride to reduce the glycogen content in the conduction system of the heart in rats.

Animals↗