[The DiaMorf-Cito telemedicine complex in the consultation-diagnosis network of the Federal Children of the North Program].
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Child↗
Biomedical subjects
I E Smirnov
Publications and source records attributed to I E Smirnov.
[Effect of coronary arterial occlusion on prostacyclin biosynthesis in dogs of various ages].
In acute experiments in animals of different age, local myocardial ischemia was stimulated, and the pattern of change in prostacyclin biosynthesis by segments of ischemized and normal coronary arteries was studied. Prostacyclin biosynthesis by coronary arterial segments was much more intensive in young animals, as compared to adult ones. Ischemized arterial segments of pups were also shown to produce a much smaller quantity of prostacyclin, as compared to control animals and to adult levels. The demonstrated findings may be making an important pathogenetic contribution to ischemic heart damage.
Age Factors↗
[Newly developed stenocardia: functional activity of thrombocytes].
Platelet function (aggregation, circulating platelet aggregates, platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-PGF1 alpha, platelet count) was evaluated in patients with angina of new onset, as compared to individuals without coronary heart disease, and patients with angina of long standing (28 +/- 4.6 months). Some of the patients with angina of new onset were examined repeatedly 6 to 12 months after the onset of angina. Platelet activity was shown to be significantly higher in patients with stable angina of new onset, as compared to patients with lasting angina, where ADP and serotonin were used as inductors. Platelet aggregation, induced by platelet activation factor and collagen, was similar in all groups. Repeated investigation 6 to 12 months after the first anginal attacks demonstrated that most of platelet functional parameters declined or tended to decline.
6-Ketoprostaglandin F1 alpha↗
[Effect of ritmilen and allapinin on prostanoid and cyclic nucleotide levels in patients with cardiac rhythm disorders].
The effect of antiarrhythmic drugs, ritmilen and allapinin, on endogenic prostanoid and cyclic nucleotide levels was examined in patients with heart rhythm disorders. Intravenous administration of antiarrhythmic agents is shown to be accompanied with increased release of prostacyclin that has antiarrhythmic properties into myocardial outflow. Both ritmilen and allapinin promoted the predominance of prostacyclin over thromboxane, with its intrinsic arrhythmogenic properties. Ritmilen- or allapinin-induced changes in prostaglandins E and F2 alpha consisted in that PGE prevailed, as compared to PGF2 alpha. There were no significant changes in cyclic nucleotide ratios (cAMP/cGMP) in response to treatment.
Aconitine↗
[Content of endogenous prostanoids in patients with paroxysmal supraventricular disorders of the heart rhythm].
Blood endogenous prostaglandins, E, F2 alpha, prostacyclin and thromboxane levels were measured in the ascending aorta and the coronary sinus of 32 patients (29 males and 3 females) with paroxysmal supraventricular arrhythmias (atrial fibrillation and supraventricular tachycardia) during the sinus rhythm and an arrhythmic paroxysm. Group 1 was made up by 22 patients with idiopathic cardiac rhythm disorders, and group 2 comprised 10 coronary patients with arrhythmias. A relationship was demonstrated between cardiac endogenous prostanoids balance and the clinical pattern of cardiac rhythm abnormality (duration and frequency of paroxysms) as well as changes in cardiac prostanoid rations associated with tachyarrhythmic paroxysms.
6-Ketoprostaglandin F1 alpha↗
[Thromboxane and prostacyclin in patients with stenocardia in induced and spontaneous ischemia of the myocardium].
The levels of TxB2 and 6-keto-PGI alpha in the coronary sinus and thoracic aorta blood were determined in 14 patients with angina pectoris and signs of coronary atherosclerosis. 12 patients were involved in a dynamic study: before, during and 10 minutes after ischaemia-inducing atrial pacing. In all the patients atrial pacing resulted in a typical episode of angina, in 7 of them ST-segment depression of not less than 2 mm was seen on the ECG. In one patient arachidonic acid metabolites were evaluated during the control period and during a spontaneous episode of angina accompanied by ST-segment elevations. In 8 of 9 patients TxB2 was produced by the myocardium during atrial pacing. During monitored evaluation of arachidonic acid metabolites one patient with spontaneous angina demonstrated a gradual lowering of the 6-keto-PGI alpha, it being minimal by the beginning of the episode; TxB2 level increased more rapidly.
6-Ketoprostaglandin F1 alpha↗
[Concentration of endogenous prostanoids and cyclic nucleotides in patients with atrial fibrillation].
The variations in the content of endogenic prostanoids and cyclic nucleotides in the blood plasma of the coronary sinus and ascending aorta were studied in patients with the idiopathic stable form of atrial fibrillation before and after sinus rhythm recovery effected by electroimpulse therapy. Changes in the levels and ratios of these compounds in the coronary venous and arterial blood were found to be opposite in their trends. A significant elevation in TxB2 levels and the TxB2/6-keto-PGF1 ratio as well as increased cGMP concentrations in the plasma of the coronary venous blood appear to be suggestive of an unfavourable prognosis because patients with such changes developed atrial fibrillation recurrences soon after electroimpulse therapy.
Adult↗
[Cardiac effects of essential phospholipids and prostaglandin release by the heart in the rat].
The article deals with the effect of exogenic phospholipids of vegetative origin enriched with polyunsaturated fatty acids (EPL substance) on prostaglandin release and the activity of the isolated, perfused according to Langendorf , heart of Wistar and Okamoto-Aoki rats with congenital arterial hypertension. Exogenic essential phospholipids were shown to facilitate a significant enhancement of endogenic prostaglandin release and to induce a positive inotropic, negative chronotropic and marked coronarodilating effects. These EPL effects were inhibited by indometacin and were considerably altered in rats with spontaneous hypertension. It was concluded that the cardiac effects of essential phospholipids are modulated by elevated prostaglandin secretion. The role of essential phospholipids in the prostaglandin biosynthesis regulation and the cardiac activity of rats is discussed.
Adenosine Triphosphatases↗
[Age-related changes in prostacyclin and thromboxane B2 biosynthesis under normal conditions and in arterial hypertension].
An experimental radioisotopic study in normotensive male Wistar rats and spontaneously-hypertensive rats (SHR) of Okamoto--Aoki line demonstrated an age-related increase in the biosynthesis of prostacycline (PGI2) from 14C-arachidonic acid by pulmonary and aortal tissues of animals with normal arterial pressure. In SHRs, PGI2 production by lung homogenates did not change essentially with age, but decreased considerably in adult SHRs with stable hypertension. PGI2 biosynthesis by SHR's aortal tissue decreased with age and dropped significantly as arterial hypertension developed. In normotensive rats, the formation of thromboxane B2 (TxB2) by platelets increased with age. Platelet TxB2 biosynthesis was elevated considerably both in young and adult SHRs. Clinically, a significant increase of platelet TxB2 production from exogenous 14C-arachidonic acid was demonstrated in children with essential hypertension.
Adolescent↗
Effect of prostacyclin on coronary blood flow and cardiac activity in normotensive and spontaneously hypertensive rats.
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Animals↗
[Effect of prostaglandins on the activity of the isolated rat heart with normal arterial pressure and spontaneous hypertension].
The article discusses the results of experimental study of the effect of prostaglandins E2, A2, and F2 alpha on coronary blood flow and contractility of an isolated and perfused after Langendorff heart of rats with normal arterial pressure. A substantial reduction of the synthesis of prostacycline and prostaglandin-like compounds in the heart of rats with spontaneous hypertension was found. Marked changes were revealed in the cardiac effects of arachidonic and linoleic acids and changes in the reactivity of the heart of rats with spontaneous hypertension to the injection of isoprenaline, oxyfedrine and verapamil. The role of changes in prostaglandin production in the pathogenesis of myocardial insufficiency in arterial hypertension is discussed.
Animals↗
[Chronoinotropic reaction of the hypertrophied myocardium using an electromechanical coupling mathematical model].
Static and dynamic chrono-inotropic responses were recorded from both normal and hypertrophic rat auricular myocardium. The slope of the static force-frequency relation from hypertrophied heart was steeper than in the control hearts. The cellular mechanisms underlying changes in the force frequency response associated with hypertrophy of the heart were studied by means of a mathematical model of excitation-contraction coupling. The characteristic features of hypertrophied heart force-frequency relations are shown to be due to the enhanced volume of the intracellular Ca-stores in contrast to the total volume of the cardiomyocyte.
Animals↗
[Changes in kinetics of deaminated biogenic amines in spontaneous hypertension].
Rate of serotonin and benzylamine deamination was increased in liver tissue of rats with spontaneous hypertension. The increase was due to elevation in Vmax value for monoamine oxidases of the A and B types as compared with the corresponding values of control animals. The Vmax value was increased in kidney of hypertensive animals for MAO of the B type (benzylamine as a substrate). At the same time, Km for MAO of the B type was increased in liver tissue, while Km for MAO of the A type was decreased in brain of hypertensive animals. Titration of the MAO active sites exhibited their increased concentration in the B type MAO in liver mitochondria of experimental animals. The data obtained suggest an important role of alterations in the MAO catalytic activity in pathogenesis of spontaneous hypertension.
Amines↗
[Production of cardiac prostanoids and the fatty acid composition of cardiac phospholipids in various types of myocardial hypertrophy].
Considerably increased production of cardiac prostanoids and intensified linoleic acid metabolism in the cardiac phospholipids were revealed in physiological myocardial hypertrophy in animals trained by swimming. The formation and secretion of cardiac prostanoids was found to be essentially reduced in pathological myocardial hypertrophy in rats with hereditarily determined arterial hypertension, which is attributed to inhibition of the metabolism of linoleic and linolenic acids in the cardiac phospholipids and to structural and functional disorders in the function of the heart.
Animals↗
[Defect in deamination of biogenic amines in spontaneous hypertension].
Activity of monoamine oxidases (MAO) of the types A and B (substrates: 5-hydroxytryptamine, 2-phenylethylamine, tyramine) has been studied in mitochondrial fractions from brain, heart, liver and kidney of 24-week-old rats of the normotonic strain Wistar Kyoto (WKY) and spontaneously hypertonic rats (SHR). As compared with the WKY rats, in the SHR strain the activity of MAO-A in heart mitochondria was increased 1.5-1.7-fold; in liver mitochondria the activities of both MAO-A and -B were increased 2.6-2.7-fold. In brain mitochondria there was noted only slight tendency towards an increase in MAO-A (substrate: 5-hydroxytryptamine) and MAO-B (substrate: 2-phenylethylamine) activities in the SHR strain as compared with the normotonic animals of the same age. However, in experiments with tyramine as a substrate of MAO the enzymatic activity in SHR brain mitochondria was increased 1.5-fold (P less than 0.05) as compared with the WKY rats. In kidney mitochondria of SHR the activity of MAO (substrates: 5-hydroxytryptamine, 2-phenylethylamine, tyramine) did not exhibit any alterations as compared with the control WKY rats.
Animals↗
[Effects of a diet with various polyunsaturated fatty acid contents on the secretion of prostaglandins and ATPase activity in the rat myocardium in total ischemia].
Experiments were made on the heart perfused according to Langendorf's method of adult Wistar and Okamoto-Aoki rats with hereditary arterial hypertension given the diets with varying content of polyunsaturated fatty acids (PUFA). It was demonstrated that under total heart ischemia, there was a maximal increase in the output of prostacycline and prostaglandin E (PGE) by the hearts of hypertensive rats given the diet enriched with linoleic acid. The rats given the PUFA deficient diet and the diet enriched with linoleic acid did not show any substantial changes in PG secretion by the ischemized heart. It was also disclosed that under normoxic perfusion, Na, K-ATPase activity in the heart of hypertensive rats was increased, being significantly inhibited during total heart ischemia. According to the authors, the differences in the changes in PG secretion and Na, K-ATPase activity might be related to a possible effect of lipid diet components and to variations in PUFA content in heart phospholipids.
Animals↗
[Effect of polyunsaturated fatty acids in the diet on prostaglandin formation and the activity of the isolated heart].
Experiments on normotensive adult Wistar rats with hearts perfused according to the modified Langendorf technique and Okamoto-Aoki rats with a hereditary determined arterial hypertension kept on the diets with varying content of polyunsaturated acids (PUFA), series 6 and 3, have demonstrated that PUFA deficiency in the diet inhibited prostaglandin (PG) secretion by the heart of hypertensive rats, which was accompanied by the decreased rate of coronary perfusion. It has also been revealed that excess content of linoleic acid in lipid fractions of the diet was followed by an appreciable rise of prostacycline secretion, whereas the linoleic acid increase in the diet by the lowering of the overall amount of PG secreted by the heart of hypertensive rats and drop of the coronary perfusion rate. It has been demonstrated that these changes might be related to the modulations in the content of PUFA, PG precursors, in heart phospholipids.
Animals↗