Biomedical subjects
Publications and source records attributed to T V Balueva.
Blockade of NO synthesis in narcotized rats potentiated pressor effects of phenylephrine by 55% and increased total peripheral resistance by 153%. Vasodilation caused by enhanced NO secretion modulated pressor shifts evoked by stimulation of alpha(1)-adrenoceptors with phenylephrine.
Systemic vasodilation produced by sodium nitroprusside in various concentrations and accompanied by a decrease in baseline blood pressure was followed by progressive reduction in pressor responses to alpha-adrenoceptor agonist phenylephrine (mesatone) in rats. In a blood pressure range of below the physiological level (80-100 mm Hg), a positive linear correlation was revealed between the decrease in baseline blood pressure and pressor effect of phenylephrine.
Blockade of NO synthesis in anesthetized rats significantly potentiated pressor responses to Polyglucin (by 70%) and considerably increased total peripheral resistance. It was concluded that vasodilatation induced by increased systemic blood flow (cardiac output) modulates pressor responses under conditions of increased blood volume.
In anaesthetised rats, bending of the body for 30 degrees and 45 degrees entailed a reverse linear dependence between the systolic and diastolic pressures under conditions of initial blood pressure over 95 mm Hg, whereas in initial blood pressure lower than 95 mm Hg the dependence is direct. In bending of the body for 60 degrees the dependence was direct and only present in initial blood pressure lower than 95 mm Hg. Pressor effects of mesaton in orthostasis directly depended on the level of the initial blood pressure. Any dependence of the cardiac output shifts on the initial blood pressure was absent. The direction and the degree of the arterial system reactivity's changes in response to orthostasis and adrenergic effect of mesaton was found to depend on the bending angle and the initial blood pressure level.
Experiments with unconscious rats showed that blocking of NO secretion intensifies orthostatic hypotension (mean arterial pressure drops by 72%) and reduces proportionally the calculated total peripheral resistance. A supposition has been made concerning involvement of the endothelial relaxing factor in orthostatic hypotension development, since in orthostasis cardiac output (systemic blood circulation) losses its influence on the endothelial NO secretion.
In anaesthetised rats, effects of blockade of the NO-synthetase upon hemodynamic shifts were studied (arterial pressure, cardiac output, general peripheral vascular resistance), the shifts being evoked either by increase (infusion of polyglucon) or by decrease (orthostasis) in the cardiac output. Under the blockade of the NO-synthetase, the pressor effects of polyglucon increased by 27% and the orthostatic hypotension by 72%. Responses of general peripheral vascular resistance changed in the same direction. The findings suggest importance of the NO secretion by the vessels' endothelium for formation of the systemic hemodynamics responses.
In anaesthetised rats, dependence of haemodynamics upon increase in the blood volume due to infusion of polyglucin in amounts 1.2 and 2.4 ml (8% and 16% of the blood volume in rats, respectively) < was studied. In the former case the initial blood pressure increased by 30%, in the latter case--by 42%; cardiac output--by 16% and 40%. The metasone pressor effects, at the were reliably decreased by 27% and 65%, and those of general peripheral resistance--by 40% and 80, respectively. The cardiac output changes did not differ significantly. The data obtained suggest an effect of the blood volume increase upon a drop of the arterial system's adrenoreactivity as a result of increase in initial blood pressure.
In anesthetized rats, a reverse linear correlation of arterial pressure (AP) shifts was found within the range of initial AP over 95 mm Hg under the head-up tilts at 30 and 45 degrees. Within the range beneath 95 mm Hg this correlation was transformed into the direct one. Under 60 degrees tilt such correlation only occurred within the range beneath 95 mm Hg. The direction and degree of the arterial system responsiveness seems to depend on the tilt value as well as on the range of the initial AP.
Reported are data of experiments with unconscious tilted rats (30 degrees, 45 degrees and 60 degrees) in which a dependence of orthostatic hypotensive reactions of systolic (APs) and diastolic (APd) pressure on spontaneous level of baseline mean arterial pressure (APb.mean) was established. Rats tilted at 30 degrees and 45 degrees, APs and APd were in inverse linear dependence with APb.mean above 95 mm Hg and in direct dependence with APb.mean below 95 mm Hg. Pressor effects of phenylephrine correlated directly and to the same extent with APb.mean only below 95 mm Hg in the 30 degrees and 45 degrees tilt and both above and below 95 mm Hg in the 60 degrees tilt. Mean values of the pressor effect before and after experiment were different in animals tilted at 60 degrees. No dependence of cardiac output on APb.mean was determined. Therefore, the trend and depth of changes in the arterial system reactivity to tilt are dependent on the degree of inclination and the APb.mean range. Reactivity to the adrenergic agent alters only when inclination is greater than 45 degrees.
A stepwise decrease in the blood pressure by means of sodium nitroprusside infusion led to progressing diminishing of mesatone pressor effects in anaesthetised rats. Cardiac output changes due to mesatone administration did not depend on the initial blood pressure. The latter being lower than physiological limits, a direct linear correlation occurred between pressor responses and shifts of general peripheral resistance, on one hand, and the degree of the blood pressure initial drop, on the other hand. The constrictor responses under study are discussed in respect to their dependence on initial tone of arterial vessels.
The effect of the elevated arterial tone on pressure responses to stimulation of arterial alpha-adrenoreceptors by phenylephrine hydrochloride was studied in anesthetized Wistar rats. Different levels of the arterial tone and, hence of the mean arterial pressure, were established by means of angiotensin II infusion in the range from 101 to 160 mmHg. An elevation of the arterial tone led to a significant reduction of the arterial pressure and peripheral resistance rise produced by phenylephrine. The degree of relative reduction of the increase in the diastolic pressure exceeded 1.3 times that in the systolic pressure. The shifts of cardiac outputs remained unchanged. After cessation of angiotensin II infusion the restoration of the arterial pressure took place almost till the initial level. At this time the pressure effects of phenylephrine were tended to recovery. It is suggested that the elevated arterial tone attenuates the systemic pressure response to stimulation of arterial alpha-adrenoreceptors by a vascular mechanism based on a transmural pressure changes evoked by the constriction of the arterial vessels.
The correlation analysis revealed no correlation within the range 110 to 80 mm Hg further transforming into a direct (within the range lower than 80 mm Hg) dependence of the pressure responses to mesatone on the reduction of initial mean arterial pressure under orthostatic hypotension in anaesthetised rats. Under paraverine hypotension a reverse correlation within the range 110-80 mm Hg transforming into a direct dependence (within the range lower than 80 mm Hg) of the responses to mesatone were observed. The dependence of cardiac shifts to mesatone on the initial arterial pressure was not occurred. The mechanisms of dependence of the systemic vascular responses on initial tone of arterial vessels, are discussed.
The correlation analysis revealed a direct (within the range 80 to 120 mm Hg) further transforming into a reverse (within the range 121 to 160 mm Hg) dependence of the blood pressure depressor shifts on the initial mean arterial pressure in anaesthetised rats. Within the physiological range of arterial pressure (70 to 130 mm Hg) there is no difference in responses to nitro-glycerine from their initial values. The mechanisms of dependence of the systemic vascular responses on initial tone of arterial vessels, are discussed.
A significant decrease of arterial pressure in response to isoproterenol occurred in anaesthetised rats with the initial pressure 101-130 mm Hg. Elevation of the initial pressure up to 131-180 mm Hg led to a significant attenuation of the depressor effect. The correlation analysis revealed transformation of direct correlation into inverse one between the depressor responses to isoproterenol and the degree of elevation of the initial arterial tone, as well as lack of such a dependence in the cardiac output shifts.
Contribution of the original angiotensin-2 controlled arterial tone to the shifts in systolic and diastolic arterial pressure (AP) was assessed in unconscious rats during tail-suspension. With this technique, values of original mean AP were elevated from 80-110 to 111-140 mm Hg. In the head-down position, rise in the tone was concurrent to a twofold increase in the number of "uncompensated" responses and a similar decrease in the number of test-resistant responses. The original arterial tone high, maximum decline of diastolic pressure was significantly less pronounced. Recovery of both systolic and diastolic arterial pressures was more dynamic against the background of high original tone. Magnitude of the diastolic AP variation dominated over that of systolic AP. These results are being analyzed in comparison with the data about orthostatic compensatory reactions.
In acute experiments with antiorthostatic rats tilt-induced changes in the parameters of cardiac activity (left ventricle systolic pressure (LVPs), its first derivative dp/dt, end-diastolic pressure (EDP) were compared in relation to the directionality and extent of systolic (sAP) and diastolic arterial pressure (dAP) shifts. Rise of the tilt angle by 15-45 degrees reduced sAP and dAP, increased LVPs and EDP and did not influence dp/dt. Changes in the cardiac parameters and AP were not unidirectional; sAP and dAP shifts were asynchronous. In a special experimental series, higher tilt angle was found to bring about opposite changes in cardiac ejection (CE) and total peripheral resistance (TPR). Growth in CE was concurrent to a progressive decline in TPR. Discussed is the response of the vascular system to antiorthostasis the unique character of which is vasodilatation.
A considerable decrease in pressor responses to polyglykine at an elevated arterial tone and constant increase of cardiac output occurred in anesthetised rats. Vascular and cardiac mechanisms of the interrelationship are discussed.
A significant decrease in arterial pressure and total peripheral resistance occurred following elevation of the initial blood pressure to 160 mm Hg with mesathone in anesthetised rats. The increase in the cardiac output remaining unchanged. Vascular and cardiac mechanisms of the revealed relationships are discussed.