Publications by authors named "Sh I Ismailov"

It has been shown that the 15-bay use of dl-propranolol (100 mg/kg a day) leads to a significant increase in the dissociation constant (CD) of the sites of specific binding of 3H-WB-4101 with membranes of rat mesenteric vessels. The concentration (Bmax) of the binding sites does not significantly change. Propranolol and other adrenoblockers do not possess any affinity for alpha-adrenoreceptors of rat brain synaptic membranes, i.

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Experiments on anesthetized rats were made to study the effects of atenolol and propranolol on cardiac output and distribution of the drugs in the heart, lungs, brain, kidneys, large and small intestines, stomach, liver and skeletal muscles with the use of radioactive carbonized microspheres techniques. Atenolol and propranolol provoked a decrease in cardiac output and raised the total peripheral resistance without a detectable effect on blood pressure. Administration of atenolol brought about a decrease in the renal blood flow whereas that of propranolol in the myocardial blood flow.

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Experiments on anesthesized normotensive rats (NR), spontaneous-hypertensive rats (SHR) and rats with experimental renovascular hypertension (RVR) were made to study the effect of prostaglandins (PG) - PGI2, PGE1, PGF2, and indomethacin on systemic hemodynamics, pressor reaction and cardiac component of the baroreflex. PGI1 (0.015 microgram/kg) PGE1 (5 micrograms/kg) produced marked hypotension which was more remarkable in RVR and SHR than in NR.

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Experiments on narcotized normotensive Wistar rats, spontaneously hypertensive rats and rats with one-kidney spontaneously hypertensive rats and rats with one-kidney Goldblatt hypertension were made to compare the main parameters of systemic hemodynamics and baroreceptor reflex function. It was shown that elevated blood pressure in hypertensive rats mainly depends on the elevation of peripheral resistance. Cardiac output determined by impedance cardiography did not differ significantly in all the three groups of rats.

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It was shown in experiments on anesthetized normotensive, spontaneous-hypertensive rats and in those with experimental renovascular hypertension (NR, SHR and RVR, respectively) that intravenous injection of bradykinin (10 micrograms/kg) produces a decrease in arterial pressure and general peripheral vascular resistance. Intra-aortal administration of bradykinin causes hypotension as well. The degree of arterial pressure lowering in hypertensive rats is far greater than in NR.

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The effect of prostaglandins (PG) E1, A1, and F2 alpha on the systemic arterial blood pressure, local brain circulation, vascular resistance and oxygen tension in the motor region of the cortex, reticular formation and ventromedial nucleus of the hypothalamus was studied in experiments on non-narcotizied rabbits. Intravenous administration of PGE1 (10 microgram/kg/min); PGA1 (50 microgram/kg/min) and PGF2 alpha (50 microgram/kg/min) produced systemic hypotension accompanied by reduction of the local brain blood flow, vascular resistance and oxygen tension in the cortex and subcortical structures. The most pronounced changes in the systemic arterial blood pressure and local brain blood flow were recorded after PGE1 administration, these changes being less marked after PGA1 and PGF2 alpha injections.

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The effect of prostaglandin E1 (PGE1) on the cardiovascular system of the dog has been studied in experiments with anesthetized dogs. After intravenous injections of PGE1 (5 microgram/kg) arterial hypotension, tachycardia, increase of cardiac output, increase of myocardial contractility were observed. PGE1 induced dilatation of pulmonary vessels.

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Intravenous administration of prostaglandin A1--PGA1 (10 gamma/kg) brings down arterial pressure, increases the rate of cardiac contractions, of cardiac output and myocardial contractility. Despite elevated pressure in the pulmonary artery the overall pulmonary resistance decreases without any substantial intensification of the right ventricle output. The mean circulation volume in the common carotid and superior mesenteric arteries shows but a momentary increase under the effect of PGA1.

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The effect of prostaglanding B1 (PGB1) on the cardiovascular system of dogs was studied in experiments on anesthetized dogs. The intravenous injection of PGB1 (40 microng/kg) was followed by aortic hypertension, tachycardia, an increase of myocardial contractility, an enhancement of minute volume of the heart, and in increase of arterial pressure in the pulmonary artery. Total peripheral resistance and total lung resistance were reduced.

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The effect of PGF2alpha on the systemic and regional hemodynamics was studied in experiments on narcotized dogs. After an intravenous injection of F2alpha (in a single dose of 10 mg/kg) aortal hypertension, tachycardia, an increased pressure in the pulmonary artery and a slightly greater cardiac output were recored. The total peripheral and pulmonary resistance was up.

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In experiments with anesthetized female-rats the influence of intravenous prostaglandins F2alpha (40 mg/kg) and Ei (10 mg/kg) on the cardiac output (by the method of dye dilution) and on the blood flow distribution among organs and tissues (by the method of Rb86 distribution) was studied. Prostaglandin F2alpha increased the arterial pressure, cardiac output along with the volume of the circulating plasma and reduced the total peripheral resistance. The hypertensive effect of prostaglandin F 2alpha is, under the circumstances, conditioned by the increased cardiac output and this substance is also instrumental in augmenting the proportion of the blood flow going to the digestive tract, skeletal muscles and, at the same time, in reducing its share flowing to the liver, spleen, skin and the uterus.

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