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Biomedical subjects

K A Merzon

Publications and source records attributed to K A Merzon.

At least 19 recordsLinked to original sources
PubMed1988

[Effect of nifedipine on renal activity].

Sublingual administration of nifedipine (N) at a dose of 20 mg to 8 persons without cardiovascular and renal pathology and to 19 patients with congestive heart failure (CHF) increased renal excretion of sodium (by an average of 51.1-132.8%), water (by an average of 31.7-101.9%), potassium (by an average of 43.2-63.2%) and calcium (by an average of 118%). The natriuretic effect of N appeared in 20 min reaching its maximum in 45-60 min, being more noticeable in CHF. An increment of natriuresis resulted from a decrease in sodium tubular reabsorption (correlation factor--0.92) rather than from an increase in glomerular filtration (correlation factor +0.50). N suppressed sodium reabsorption in the proximal tubule (by an average of 34.1%) as well as in the segment, more distal of Henle's loop (by an average of 6.8%). N might suppress directly calcium-dependent mechanisms of sodium transtubular transport but it could also produce a mediated effect as a result of shifts of renal hemodynamics.

Diuresis↗
PubMed1988

[Assessment of the calcium homeostatic state using the double calcium tolerance test].

An acute tolerance test per os using calcium (Ca) lactate at a dose of 0.25 mmol of Ca per kg of body mass (calcium tolerance test--CTT) was performed twice in healthy persons (HP) and in patients with chronic heart failure (CHF) of various degrees: before and after 3-day administration of the same dose of Ca lactate. The "double" CTT made it possible to detect in HP and CHF a "phenomenon of adaptation" to Ca excess in the body based probably on changes in the activity of calcium-regulating hormones. It was manifested in less marked and prolonged tolerance hypercalcemia and a more rapid and effective calciuretic reaction, and probably in decreased intestinal absorption of Ca. It pointed to reversibility of Ca metabolic derangements even in severe CHF and a possibility of their non-medicamentous correction.

Calcium↗
PubMed1987

[The possibility of targeted pharmacological action on the intravascular binding of calcium ions: a new aspect of pharmacodynamics?].

The administration of cardiac glycosides (digoxin, strophanthin, corglycon) invariably produced a calcium ionizing effect raising the content of blood serum ionized calcium and a degree of serum calcium ionization. Calcium transport antagonists (verapamil, nifedipine) made a reverse effect (a calcium-binding effect). Both effects were noted 5-15 min, after administration of the drugs disappearing in 60-90 min. They were reproduced after adding digoxin, strophanthin and verapamil to the blood serum in vitro but they were not summarized and probably did not depend on a basal level of calcemia. Under the influence of digoxin blood serum calcium binding capacity was on a regular decrease whereas under the influence of verapamil and nifedipine it was on an increase. Close negative correlation was found between shifts of blood serum calcium binding capacity and a degree of serum calcium ionization.

Calcium↗
PubMed1986

[Fractional composition of serum calcium in chronic heart failure].

The total calcium concentration (Cat) using an atom-absorption spectrophotometer and ionized calcium concentration (Ca2+) with ionoselective electrodes were determined in the blood serum of 28 healthy persons and 159 patients with chronic cardiac insufficiency (CCI). The blood serum Cat concentration in CCI decreased clearly in parallel with its gravity. Ca2+ concentration remained within normal fluctuations shifting to their low border ("hypocalcemia within normal"). These shifts of the calciemia fractional composition were determined by a decrease in the calcium-binding capacity (CBC) of serum buffers resulting in a decreased portion of the physiologically inert nonionized (bound) fraction in Cat. Cat concentration grows with the effective treatment of CCI, perhaps as a result of the normalization of CBC.

Calcium↗
PubMed1985

[Effect of verapamil and nifedipine on the fractional composition of calcium in the blood serum].

A single administration of verapamil (5 mg infused intravenously) and nifedipin (20 mg sublingually) in 31 patients with chronic cardiac failure of stage I and IIA decreased the levels of ionizing calcium (Ca2+) in the blood serum (the maximum reduction averaged 19.8% and 16.8%, respectively). The total concentration of calcium (Ca0) in the blood serum did not alter, so the degree of ionization of the serum calcium (Ca2+/Ca0) decreased. This effect was felt 5 min after verapamil administration and 15 min after nifedipin administration, generally reaching the peak in 30 min and somewhat subsiding in 60 min. The nature and time-course of changes of Ca0 and Ca2+ in the blood serum following the drug administration suggest that they are induced by a transient increase in the Ca-binding capacity of the serum buffers, i. e. they are realized on the physicochemical level. This effect shows no tendency to cumulate following a prolonged (1.3-15 months) administration of the above drugs. The coefficients of the paired correlation between the shifts in the Ca2+ content on the one hand and hemodynamic parameters on the other indicate no significant correlation between them. However, the author believes that the consistent decrease in the Ca2+ concentration in the blood serum is involved in the pharmacodynamics of verapamil and nifedipin.

Calcium↗
PubMed1985

[Calciuretic function of the kidneys in chronic cardiac insufficiency].

Excretion of calcium (Eca) with the kidneys decreases parallel with progress of chronic heart insufficiency (CHI). In stage III CHI, the daily Eca constitutes 25.4% on the average of normal. The reduction in calciuresis is about to an equal extent determined by hemodynamic disorders, drop of glomerular filtration, and increase of tubular calcium reabsorption. Inhibition of tubular calcium reabsorption is the decisive factor that determines the degree of the calciuretic response after oral intake of calcium lactate. Insufficient inhibition of tubular calcium transport, as compared to controls, accounts for a decrease in the calciuretic response to the intake of calcium lactate in patients with CHI. It is assumed that the increased tubular calcium reabsorption is caused by the action of some extrarenal regulatory factors that reduce the ability of CHI patients to resist external excess calcium supply.

Calcium↗
PubMed1983

[Use of antipotassiuretic diuretic amiloride in patients with chronic cardiac failure].

Amyloride causes moderate natriuresis and a considerable reduction in urinary potassium excretion. Chlorine excretion and diuresis are less affected in their increase, while hydrogen ions secretion shows a slight decrease. Amyloride effect is localized in convoluted tubules of the kidney, and perhaps collecting tubules as well. When taken orally, its effect becomes evident within 2-3 hours, reaches its peak within 5-6 hours, and slowly declines within 16-18 hours. A daily dose of 10-15 mg is recommended. During a treatment course, the effect is in evidence throughout the whole of the 6-8 days of observation, without any signs of hyperpotassemia or shifts in acid-base balance. Amyloride combined with furosemide, uregit or hypothiazid produces an additive effect on natriuresis and essentially reduces renal loss of potassium and hydrogen ions.

Amiloride↗