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Biomedical subjects

R S Khrustaleva

Publications and source records attributed to R S Khrustaleva.

16 recordsLinked to original sources
PubMed2005

Effect of clonidine on potential-dependent sodium currents in sensory neurons.

In experiments on rat pups we studied the effect of clonidine on potential-dependent Na+ currents in dorsal root ganglia by the voltage clamp method. Clonidine decreased the amplitude of tetrodotoxin-sensitive and tetrodotoxin-resistant sodium currents. The range of acting concentrations and the absence of modulatory effect of norepinephrine on the efficiency of clonidine-induced blockade of sodium currents suggest that this blockade results from a direct interaction of clonidine with sodium channels.

Analgesics↗
PubMed2005

Inhibitory effect of clonidine on cholinergic transmission.

Equilibrium geometry and electronic structure of three local anesthetic molecules and clonidine were computed. It was shown that clonidine molecule could incorporate into local anesthetic binding centers in potential-operated Na+ channels and in ionic channels coupled to nicotinic cholinergic receptors. The modulatory effect of clonidine on contractile responses of skeletal muscle showed that blockade of Na+ channels and nicotinic cholinergic receptors is a part of its analgesic action.

Adrenergic alpha-Agonists↗
PubMed2000

[Study of tonic and evoked electrical activity in efferent fibers of the sympathetic nerve in white rats].

In anaesthetised Wistar rats, electrical sympathetic activity and a somatosympathetic reflex in the cervical sympathetic trunk elicited by a single electrical shock to forelimb or hindlimb afferent nerves, were recorded. The spontaneous activity was shown to conform with the pulse and respiratory waves of arterial pressure. Somatosympathetic reflex consists of early and late discharges evoked by somatic myelinated afferent fibres stimulation, and C-response elicited by stimulation of unmyelinated afferent fibres in spinal nerves.

Animals↗
PubMed1999

[Arterial mechanoreceptor reflex as a factor for execution of hypertensive responses to disturbing effects].

It has been shown in experiments on conscious cats and rats that arterial mechanoreceptor reflex is inhibited during averse emotional influence, and the changed reflex is a cause of elevation in arterial pressure. In one's turn the hypertension contributes to entry of blood plasma norepinephrine into brain and in this way increases the arterial baroreceptor reflex after the emotional influence is stopped. The augmentation of baroreflex promotes restoration of homeostasis after cessation of the stress situation.

Animals↗
PubMed1996

[The possible mechanism of the noradrenaline enhancement of the arterial baroreceptor reflex].

In anaesthetized cats intravenous infusion of norepinephrine induced the increase in arterial pressure and suppression of renal nerve electrical activity. The latter followed the infusion was stopped and arterial pressure returned toward control. The baroreflex suppression of sympathetic activity associated with norepinephrine increased in the case of preliminary mechanical damage to blood-brain barrier. Duration and intensity of the sympathetic activity suppression following norepinephrine infusion depended on the magnitude of hypertensive reaction and the rate of elevating in arterial pressure under the action of norepinephrine. Norepinephrine at the similar concentrations did not depress sympathetic activity if the arterial pressure was stabilized on the resting level. These data support the supposition that the elevation of arterial pressure due to norepinephrine infusion increases the ability of catecholamine to enter brain and in this way activates the central limb of arterial baroreceptor reflex.

Adrenergic alpha-Agonists↗
PubMed1991

[The age-related characteristics of changes in osmotic and ionic homeostasis in spontaneously hypertensive rats].

The 3-month old SHR differ from the WKY rats in that the former have an increased osmolality, concentration of albumins, activity (but not the concentration) of sodium and a reduced activity of potassium. The shifts in the albumins concentration occur, mainly, on account of the amino acid phenylalanine. The gradient increase of the sodium and potassium concentration between the plasma and muscular tissue in followed by a slight hyperpolarisation of the muscle fibers, a drop in the lability and a increase in pO2. The above shifts of homeostatic parameters were not revealed in the SHR and WKY rats of 1.5 and 6.0 months of age.

Aging↗
PubMed1991

[An analysis of the mechanisms enhancing arterial baroreceptor reflexes during noradrenaline infusion].

In cats-recipients with cut vagosympathetic trunks and hemodynamically isolated carotid sinuses, the latters were perfused with the blood from a cat donor. Noradrenaline infusion did not change the electrical activity of the renal nerve and induced an inhibition of the activity in high perfusion pressure. Noradrenaline seems to induce a short-term enhancement of arterial baroreflexes and to potentiate the effect on the central link of the reflex arch.

Animals↗
PubMed1990

[Potassium distribution in rat tissues in relation to its concentration in the blood].

The dynamics of distribution of potassium and sodium among the blood plasma and the tissues (muscle and liver) was studied in Wistar rats at an artificial increase of the potassium content in the blood. After administration of 1.25% solution of potassium chloride into the stomach (5 ml/100 g), into the liver portal vein (0.5 ml/100 g), and into femoral vein (0.1 ml/min during 45 min), the changes of potassium and sodium contents were opposite in the blood plasma and in the tissues under study. The maximal shift of these ions concentration in the plasma and tissues occurs sooner after administration of potassium directly into the blood. In continuous administration of the solution the potassium concentration reaches 10.8 mM/l in the blood plasma and returns to normal values within 2 hrs after cessation of the administration. Therefore, the redistribution of potassium between extra- and intracellular fluid plays a major role in restoration of the potassium homeostasis.

Animals↗
PubMed1990

[The participation of arterial baroreceptor reflexes in the prolonged inhibition of the electrical activity of the sympathetic nerves].

In immobilised male cats, arterial and venous pressure, heart rate and electrical activity of the renal nerve were recorded during i.v. infusion of noradrenaline at a constant initial level of arterial and venous pressure. The electrical activity of the renal nerve was inhibited and the heart rate decelerated, the obviousness of these effects increasing with acceleration of the infusion rate. The bradycardia was transient in anesthesia. The section of both vago-sympathetic trunks prevented the bradycardia and weakened the inhibition of the renal nerve activity. Additional denervation of both carotid sinuses eliminated the inhibiting effect of noradrenaline. Possible mechanisms of the noradrenaline effects are discussed.

Afferent Pathways↗
PubMed1988

[Analysis of compensatory mechanisms of arterial hypertension in norepinephrine infusion].

The NA infusion induced a raise in the AP, inhibition of sympathetic vasomotor activity and a drop in the heart rate in alert male cats. The hypertensive effect of the NA was weakening during first 90 min of the infusion, a complete inhibition of sympathetic activity persisted during the whole period of infusion as well as a decrease in the heart rate, in anesthetized cats. After deafferentation, the markedness of the arterial hypertension weakening decreased and the effect of the infusion on sympathetic activity and heart rate was abolished. Administration of pentamine during the infusion did not affect the AP in anesthetized cats, increased it in alert animals and decreased the AP in deafferented cats. The organism seems to have no humoral mechanisms of compensation of arterial hypertension induced with the 3-hr infusion of noradrenaline.

Animals↗
PubMed1987

[Erythrocyte membrane permeability of monovalent cations in rats with spontaneous arterial hypertension].

Intraerythrocyte Na and K concentrations were not different in spontaneously hypertensive rats (SHR) from those of normotensive rats (WKY). During incubation of the cells in LiCl solution for 24 h at 2-4 degrees C Li accumulation and K efflux in erythrocytes of SHR were higher as compared to WKY. A positive linear correlation was found between influx of Li and efflux of K in the erythrocytes. Li efflux from the erythrocytes at 37 degrees C was independent of the presence of a Na medium that indicated the absence of Na-Li countertransport in rat erythrocytes. There was no difference in Li efflux in both rat groups. The results provide further evidence in favor of the hypothesis of increased passive permeability for monovalent cations in erythrocytes of SHR.

Animals↗
PubMedDate not supplied

[Study of the central and peripheral mechanisms in enhancement of arterial baroreflex in cats during noradrenaline infusion].

An increased suppression of electrical activity of the cardiac inferior nerve by the baroreflex during norepinephrine infusion can be eliminated by a preliminary infusion of monoamine. The data obtained corroborated our previous findings that an increase in arterial pressure due to norepinephrine infusion was essential for catecholamine increasing the baroreflex inhibition of electrical activity in sympathetic nerves.

Animals↗