[Effect of obzidan on the function of endocrine glands regulating calcium metabolism in patients with ischemic heart disease].
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Biomedical subjects
Publications and source records attributed to G K Zoloev.
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In 140 white male rats, effects of lei-enkephalin synthetic analogue and adrenaline on heart rate, cAMP concentration in the heart and liver, glycogen concentration in the liver, parathormone content in the blood plasma, were studied. The lei-enkephalin analogue was shown to hinder the changes of these parameters induced with adrenaline. Enkephalins seem to suppress the effect of catecholamines upon adenylatcyclase and to reduce the cAMP level in tissues.
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The effect of a synthetic analogue of encephalin was studied experimentally in 150 rabbits with neoepinephrine-induced myocardial necrosis to whom the drug was administered intravenously at the rate of 100 micrograms/kg, 1 and 6 hours later. Necrotic developments were assessed on the basis of MB CPK and LDH activity and myoglobin levels. Control animals received saline solutions or propranolol in equimolar doses. In encephalin-treated animals, enzyme activity and myoglobin values were significantly lower, an evidence of encephalins' favorable effect on the course of neoepinephrine-induced myocardial necrosis.
An experimental study in rats demonstrated that myocardial infarction, induced by the ligation of the descending branch of the left coronary artery, led to marked metabolic disorders, such as increased lactate and glucose levels and decreased levels of blood calcium and magnesium and hepatic glycogen. A stable analogue of leu-enkephalin administered to the animals normalized metabolic parameters and improved the course of experimental myocardial infarction in rats.
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Stable derivative of Leu enkephalin, intravenously administered into rabbits and rats, decreased the rate of activation of creatine phosphokinase, aspartate- and alanine transaminases as well as corrected hypomagnesemia and the deteriorations in blood plasma osmolarity caused by novodrin necrosis of myocardium. The data obtained suggest that enkephalins appear to influence the system of cyclic nucleotides in myocardium.
Intravenous injection of parathyroidine to intact rats in a dose of 2 Units/100 g bw provoked a hypotensive effect. The blockade of alpha-adrenoreceptors did not change the effect of parathyroid hormone. The stable analog of leu-enkephalin inhibited the parathyroidine-induced increase in cAMP level in the vascular wall with no influence on the hypotensive action of parathyroid hormone. Since the hypotensive action of parathyroidine was blocked with isoptin, it is concluded that parathyroid hormone primarily influences sodium-calcium metabolism in the vascular wall.
The experiments with albino rats, Wistar rats and SHK mice showed that the combined use of amphotericin B and diacarb markedly potentiated the effect of the latter: the amount of the urine excreted within 6 h and the renal excretion of sodium ions increased 1.8 and 1.5 times, respectively. Analogous trends were observed in the experiments with stabilization of the animal water balance by 2 per cent water loading. The studies on rats with Pliss lymphosarcoma showed that the diuresis level in the tumor-bearing animals was 3 times lower than that in healthy rats. The treatment with 5-fluorouracil lowered this index more significantly. With the use of amphotericin B, diacarb and their combination the urination level came to normal. The cyclophosphamide therapy of mice with sarcoma 180 was accompanied by accumulation of water in the tumor tissue. The combined use of the cytostatic with the polyenic antibiotic and diuretic resulted in a significant lowering of this index. In rats with Walker-256 carcinosarcoma, the treatment with the above three drugs lowered the sodium ion concentration and increased the calcium ion concentration in the tumor tissue. At the same time the electrolyte level in some organs not affected with malignant tumor (spleen, thymus, liver and adrenal glands) returned to normal.
Experiments were made on 187 white rats weighing 180-200 g. Acute myocardial ischemia was simulated in 137 animals. Fifty sham-operated rats served as control. Experimental acute myocardial ischemia was accompanied by an increase in blood creatine phosphokinase and lactate dehydrogenase activity as well as by an elevation of serum lactate level and fall of blood plasma calcium concentration, suppression of diuresis and excretion of calcium with urine. Intraperitoneal injections of parathyroidine to rats with acute myocardial ischemia led to rapid normalization of the homeostatic parameters. Lethality of experimental animals decreased 1.8-fold.
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Plasma levels of immunoreactive parathyroid hormone and total as well as ionized calcium were measured in 18 patients with myocardial infarction on days 7 and 20-25 of the disease. An experimental study in 90 white rats was designed to determine bodily requirement of parathyroid hormone and specify its role in the genesis of hypocalcemia. On day 7 of acute myocardial infarction, the patients showed decreased plasma levels of total and ionized calcium, and their parathyroid hormone levels dropped simultaneously. The experimental study in parathyroidectomized rats with simulated myocardial infarction demonstrated that the hormone requirement grew during the acute stage of infarction. On days 20-25, the myocardial infarction patients showed an increase in total and ionized calcium, yet their parathyroid hormone levels continued to decline, a fact attributable to functional exhaustion of the parathyroid glands.
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Experiments on rats have shown that administration of a synthetic analog of leucine enkephalin at a dose of 100 mg/kg did not change the content of the immunoreactive parathyroid hormone in the blood plasma, but eliminated the parathyroidin-stimulating effect on the cAMP concentration in the renal tissue and AP activity in the blood. We conclude that enkephalins do not influence the secretion and metabolism of the parathyroid hormone, but block its peripheral effects and stimulate thyroid C-cell function.
The authors examined 56 patients with obliterating diseases (OD) of arteries of the lower extremities and conducted experiments on 97 male albino rats. In patients with OD the lactate content in the regional venous blood of the involved extremity increases proportionally to the severity of ischemia. No essential changes occur in the concentration of ATP and glucose. In rats with transitory ischemia of the extremities the lactate level in venous blood increases in the absence of changes of the ATP and glucose content; reduced concentration of ATP and glycogen was encountered in the ischemic muscles of the extremities. The mechanisms and significance of the disorders of metabolic parameters in ischemia are discussed.