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N N Samoĭlov

Publications and source records attributed to N N Samoĭlov.

7 recordsLinked to original sources
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

[Influence of the functional state of the endocrine glands on the toxicity and accumulation of lithium in rats].

Hypophysectomy, adrenalectomy, introduction of desoxycorticosterone-acetate (DOCCA) and aldosterone facilitate cummulation of lithium in the organs and plasma of rats subjected to the action of lithium chloride, whereas thyroidectomy, administration of triiodothyronine, hydrocortisone and aldactone fail to influence this process. The toxicity of lithium chloride for animals increases with hypophysectomy and adrenalectomy, remains unchanged with introduction of DOCCA, triiodothyronine and thyroidectomy and subsides under the effect of hydrocortisone.

Adrenalectomy↗
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

[Influence of lithium chloride on lipid metabolism].

Lithium chloride was injected subcutaneously to mice (in amounts of 500 and 300 mg/kg) once a day for 10 and 15 days, and to rabbits in single doses via a tube into the stomach (in amounts of 400 and 850 mg/kg). After different time intervals following a single or course-wise administration of the compound the level of total lipids was determined in the muscles and liver of the mice, and of the total lipids, beta-lipoproteins, phospholipids, cholesterol, fatty acids and 11-oxycorticosteroids levels in the blood serum of rabbits and of the bile acids content in the vesical bile of these animals. Hyperlipemia that developed under the effect of lithium was caused by mobilization of fat from fat depots and by deranged interstitial lipids metabolism.

11-Hydroxycorticosteroids↗
PubMedDate not supplied

[Toxicity of lithium salts in combined use with neuroleptics].

Experiments on white mice showed that in combined administration of LD16, LD50 or LD84 of aminazin, triphtazine or haloperidol with the same doses of lithium carbonate, chloride or hydroxybutyrate, the lethal dose exceeded the total lethal dose in the event the drugs were administered alone. Non-lethal doses of the lithium salts produced no effect on LD16, LD50 and LD84 of triphtazine and haloperidol, but non-lethal doses of these neuroleptics potentiated the action of lethal doses of the lithium salts. Haloperidol is an exception to the rule since it did not exert such action with respect to lithium chloride. Aminazin and lithium salts increased also each other's toxicity in instances where one of the drugs was administered in a non-lethal dose, whereas the other in a lethal one.

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↗