T. V. Balueva

Reactivity of Arterial Vessels during Antiorthostasis and Systemic Hypotension

In experiments on rats, changes in blood pressure and cardiac output in response to antiorthostatic (head-down) tilt 15° and 45° were examined under conditions of decreased arterial tone induced by sodium nitroprusside. The decrease in initial systemic blood pressure to 90 mm Hg attenuated the pressor responses to antiorthostasis, while further drop in blood pressure to 70-60 mm Hg provoked depressor responses in half cases. No blood pressure responses to antiorthostasis were observed when blood pressure dropped to 50 mm Hg. Correlation analysis confirmed the existence of a direct dependence of pressor responses to orthostasis on the initial blood pressure.

Involvement of nitric oxide in the mechanism of adrenergic responses of systemic circulation

Increased pressor response to the infusion of α1-adrenoceptor agonist phenylephrine was observed in conditions of inhibited NO synthesis: the mean blood pressure increased from 33.7 to 41.1% and the total peripheral resistance increased from 6.8 to 22.0%. The effect of vasodilation induced by NO secretion in the vascular endothelium after the stimulation by α1-adrenoceptors on the degree of pressor changes and changes in the total peripheral resistance is proposed.

NO-dependent mechanism of adrenergic reaction of systemic hemodynamics.

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 α1-adrenoceptors with phenylephrine.

Mechanisms of Responses of Systemic Circulation: Role of the Endothelial Factor of Vascular Tone Control

Experimental data on the effect of NO synthase inhibition on hemodynamic changes (blood pressure, cardiac output, and peripheral resistance) induced by an increased (polyglucin infusion) or decreased (orthostasis) cardiac output are presented. Under conditions of NO synthase inhibition, the pressor effects of polyglucin and orthostatic hypotension increased by 70 and 72%, respectively. The response of peripheral resistance had a similar trend. Significance of NO secretion by vascular endothelium for the development of systemic hemodynamic responses is proposed.

Effect of baseline vasodilation on adrenergic reactions of systemic hemodynamics.

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 α-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.

Role of Endothelium-Dependent Mechanism in Formation of Systemic Hemodynamic Responses to Hypervolemia

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.

Role of adrenergic innervation in distribution of systemic and coronary fractions of left ventricular ejection with raised intraaortic pressure

Acute experiments were carried out on cats anesthetized with chloralose (50 mg/kg) and pentobarbital (20 mg/kg), with an open chest and artificially ventilated. SF of the left ventricular ejection was judged on the basis of measurements of volume velocity of blood flow in the ascending aorta (distally to the origin of the coronary arteries) by means of a vascular transducer (diameter 7 mm) of an RK~-2 electromagnetic flowmeter. CF was determined by measuring the outflow from the coronary sinus, multiplied by 3/2, by the method described previously [2, 3]. The intraaortie systolic pressure (AP I) was gradually raised by increasing the resistance in it with an occluder, located distally to the transducer of the electromagnetic flowmeter (Fig. i). The occluder consisted of a loop, wrapped around the ascending part of the aorta, and a micrometer system. The thread consisted of Kapron tape 0.8 mm in diameter. Successive adjustment of the micrometer system by 1 mm led to an increase of AP l by 1.5-60 mm Hg. The results were grouped on the basis of levels of all parameters corresponding to a rise of AP 1 by 30 mm Hg. The results of elevation of the intraaortic pressure were analyzed before andduring ~-adrenoreceptor blockade within the same pressure ranges. AP I was recorded proximally to the site of the occluder, through a catheter (diameter 0.6-1 mm), passed through the right carotid artery to the base of the aorta. The systemic blood pressure in the femoral artery (AP 2) was recorded simultaneously. Contractility of the heart was estimated by recording the first derivative of intraventricular pressure (dp/dt max), by means of an MN-7M analog computer, on the systolic pressure curve in the left ventricle, and the end-diastolic pressure (EDP) in the left ventricle also was recorded. The degree of filling of the ventricle also was judged from the measurements of the last parameter. Pressure in the left ventricle was measured by means of a catheter passed through the auricle of the left atrium. All pressures were recorded by means of a pressure transducer of the PDP-400p type. All parameters were recorded simultaneously on N-3021 and N-338 automatic writers. The results were subjected to statistical analysis by Students t test. The

Correlation between systemic and coronary fractions of left ventricular ejection during pressor reflexes

-adrenoreceptors of the heart and vessels were blocked by propranolo~ injected in a dose of 1 mg/kg into the animals femoral vein.

Role of the cardiopulmonary blood volume in changes in left ventricular output during stimulation of somatic afferent nerve fibers

During excitation of the sympathetic nervous system induced by blocking of the carotid sinus baroreceptors or by stimulation of afferent C-fibers of a somatic nerve, leading to pressor reflexes of the arterial blood pressure (BP), various changes are observed in the cardiac output. The writers showed previously that during these pressor reflexes, at the stage of the transition process disparity is observed between the return blood flow into the right atrium and the left ventricular ejection (LVE) [5, 6]. One factor determining this disparity in our experiments may have been the extent of the coronary blood flow (CBF), which was disregarded when the cardiac output was recorded in the ascending aorta. The role of the coronary factor likewise was disregarded by other investigators [i0, 14, 15], who also recorded cardiac output (CO) in the ascending aorta. It was thus impossible to estimate the total LVE (COrot) , which is equal to the sum of the systemic and coronary fractions (SF and CF respectively), and this may have been the reason for the contradictory interpretation of changes in the pumping function of the heart during pressor reflexes. The suggestion that CBF is important when these changes are assessed was put forward previously [3, 8]. An increase of pressure in the aorta leads to an increase in the coronary perfusion pressure, and in turn, during the transition process, this leads to a change in CBF and the blood volume in the coronary bed. Autoregulation of CBF is exhibited only in the steady state [9]. Interest in the role of the coronary factor can also be attributed to the fact that it is not only the mechanical activity of the heart and the level of its metabolism in the heart--coronary vessels system that determines the value of CBF, but, as many other investigators have shown [4], the opposite dependence also applies -coronary inotropic influences on the heart, changing its output.

Analysis of factors determining changes in cardiac output in reponse to catecholamines

UDC 612.178 Vessels of the pulmonary circulation contain about 20%, and the right and left chambers of the heart up to 10% of the circulating blood volume [5]. Investigations on dogs have shown [7] that during the first 5-6 min of muscular work the deficiency of the venous return to the heart is concealed mainly by the pulmonary reserve and the end-systolic volume. The main source responsible for the change in left ventricular output is the functional residual capacity, which amounts to between 46 and 65% of its diastolic volume, and consists of the reserve and residual volumes [4]. The increase in stroke volume during muscular work in the period preceding the increase in the venous return to the heart takes place on account of the reserve volume [7]. During muscular work activation of afferent fibers of groups Ill-IV (mainly of type C) of somatic nerves, which react to high-voltage and high-frequency stimulation [9], takes place. Muscular contraction is essential for activation of muscle afferents [8]. The writers showed previously [3] that during the pressor response to stimulation of afferent C-fibers of the tibial nerve, the left ventricular output (LVO) exceeded the venous return to the right atrium in one-third of the experiments. However, the degree of participation of the blood volume in the pulmonary vessels and in the right ventricle and right atrium in the formarion of the inflow of blood to the left ventricle during coupled reflexes has virtually not been studied. An incre~ ~ in the blood volume in a lobe of the lung has been demonstrated [I] during stimulation of the cen~l end of the divided tibial nerve. The aim of this investigation was to study the importance of the capacitive properties of the pulmonary vessels and chambers of the right heart, and also of neurogenic influences on the right ventricle for changes in LVO in response to electrical stimulation of C-fibers of a somatic nerve. For this purpose the character and magnitude of synchronized changes in blood flow in the ascending aorta, pulmonary artery (PA), and posterior vena cava (PVC) were compared.