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Logical foundations of classical bulbar vasomotor center theory, experimental evidence on spinal localization of amphibian vasomotor center and results of electrophysiological investigation of the late components of somato-vasomotor reflexes in mammals provided basis for a new concept of the mammalian vasomotor center presenting this center as a functionally single system of spinal and bulbar mechanisms. According to this concept, phylogenetically ancient functions of the spinal part of that system (generation of tonic discharges of vasoconstrictor neurons and their reflex reactions to spinal afferent's signals) are maintained and controlled by the bulbar part, i.e. by autogenetically active neuronal circuits as well as by own afferents of the bulbar part of this single system.

In anesthetized curarized cats the degree of specialization of the descending sympathoexcitatory axons which activate sympathetic preganglionic (vasomotor) B2--neurons of the lateral horn, was studied. These sympathoexcitatory fibers with conduction velocity of 4.0--8.9 m/sec activate especially onlg the sympathetic B2--units of the spinal cord. Other neurons (phrenic and intercostal mofoneurons and sacral parasympathetic preganglionic neurons) are activated by different groups of descending fibers with conduction velocity greater than that of descending sympathoexcitatory fibers.

Vasomotor reactions to the increase of systemic blood flow by 100 ml/min occurred in anesthetized cats with left ventricular bypass: the increase of the pulsatile flow produced reflex vasodilatation, while its reduction to the initial value entailed vasoconstrictor reflex. In case of pulsatile perfusion responses of resistance vessels to the same change of systemic flow included opposite reflex and myogenic factors. Inhibition of the systemic myogenic vascular tone in absence of pulse alterations of pressure and flow is discussed.

In acute experiments on cats, the magnitude and type of responses of hindlimb accumulating vessels and of those responsible for pressure stabilization, to pressor reflexes were studied under normal conditions of the vasomotor center and after brain sections at different levels (decortication, decerebration, spinalization) as well as after occlusion of femoral or cava posterior vein. A considerable increase of arterial vessels responses to pressor reflexes occurred after decerebration at the intercollicular level whereas occlusion of the femoral or cava posterior veins led to a significant decrease of the responses. The reactions of venous vessels were constant owing to the specific features of their central regulation. Only efferent impulses to arterial part of the vascular bed seem to change under these conditions while modification of "venous" part of the efferent patterns occurred, probably, at the spinal cord level.

In anesthetized cats under conditions of acute overheating, resistance to the blood flow increased in arteries of the small intestine whereas compliance of the postcapillary vascular bed reduced in respective linear dependence. The correlation-regression analysis indicated a close linear dependence between changes in arterial vessels of the small intestine to heating and their responses to the pressor carotid sinus reflex. The mechanism responsible for splanchnic vasoconstriction under conditions of acute overheating of the organism seems to involve increased efferent impulses activity mediated by the adrenoreactive structures.

In acute experiments on cats, administration of hexonium (2 mg/kg) abolishes constrictory responses of the spleen resistance vessels in pressory sinocarotid reflex while the constrictory and dilatory responses of the capacitance vessels are preserved. Simultaneously, the high amplitude (over 15 mcV) sympathetic discharge is abolished in the spleen nerves which suggests its connection with the resistance vessels' responses, and the low-amplitude (up to 15 mcV) discharges are preserved. The reflex changes of these discharges' frequency are correlated in direction with the reflex responses of the capacitance vessels.

In acute experiments on cats, responses of the resistance and capacity vessels of small intestine, spleen, kidneys, and m. gastrocnemius were studied during pressor sinocarotid reflex and electrical stimulation of the sciatic and brachial afferents. It was shown that, against the background of constrictory responses of the resistance vessels in these organs, both the constrictory and the dilatory responses of the capicitance vessels could occur or not. Correlation analysis revealed no dependence between the markedness and character of the capacitance vessel responses and the changes of the venous blood oxygenation during pressor reflexes. The regulatory mechanisms determining, different characters of the capacitance vessels during neurogenic effects and the methodical conditions revealing the true nature of changes occurring in the postcapillary bed, are discussed.

The localization and conduction velocities of descending pathways which activate the different groups of sympathetic preganglionic nerons were studied in the cat cervical spinal cord. Certain evidences have been obtained that the fibres located near the dorsal surface of the dorsolateral funiculi with conduction velocities about 24--29 m/sec. can activate the ventral horn preganglionic neurons monosynaptically. In contrast to previous ideas, the sympathetic preganglionic neurons of the lateral horns seem to be activated not by different but by a single group of descending fibers with the conduction velocity 4--8.9 m/sec and localization in more ventral portions of the dorsolateral funiculus. The transmission from these fibers to the sympathetic preganglionic neurons of the lateral horns occurs in two ways: oligosynaptically (probably, disynaptically) and polysynaptically through a more complicated interneuronal chain. The sympathetic preganglionic neurons with unmyelinated axons, localized in the intermediate zone, for the first time were shown to be activated polysynaptically, probably via the same ways as the lateral horn neurons.

The interaction between the descending sympathoexcitatory "vasomotor" and the inhibitory baroreceptor systems was studied in cats. The spontaneous activity and reflex discharges of the identified bulbar sympathoexcitatory neurons were unaffected during the stimulation of baronlferents and the elevation of the arterial blood pressure. It was found that baroreceptor impulses inhibit the spinal interneuron system which take part in transmission of descending sympathoexcitatory influences.

The influence of low- and high-frequency stimulation of anterior, tuberal and posterior hypothalamic areas on the spontaneous rhythmogenesis in the ureter smooth muscles and on arterial blood pressure, was studied in anesthetized cats. High-frequency stimulation of all hypothalamic areas induced pressor responses with activating effects on motor activity of the ureter. The changes in the ureter rhythmic activity were synchronous with those of systemic arterial blood pressure. The low-frequency stimulation induced both pressor and depressor responses in different proportion. The depressor responses were not accompanied by any changes of the ureter rhythmic activity. Possible mechanisms of reversal of vasomotor responses in stimulation of hypothalamus, organization of sympathico-activating and sympathoinhibitory mechanisms and hypothalamic regulation of rhythmogenic function of the ureter, are discussed.

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.

In acute experiments on cats, responses of the resistance and capacitance vessels of the spleen and hindlimbs to local electric stimulation of the medulla oblongata, of the sympathetic nerves, and pressor reflexes during different pressure of the venous outflow, were studied. No structures were revealed which could selectively affect the capacitance vessels. The bulbar structures affected both the resistance and the capacitance vessels. The reflex responses aof the pre- and post-capillary portions of the vascular bed could be different, the transmural pressure being one of the factors for dilatory responses of the capacitance vessels. The different responses of the capacitance vessels could occur on account of both local and central mechanisms, their participation, however, being unequal.

The influence of low- and high-frequency stimulation of cortico-medial, baso-lateral and central nuclei of the amygdala was studied in anesthetized cats by means of recording arterial blood pressure and electrical activity of the amygdala. The induced vasomotor effects were compared with the effect of hypothalamic stimulation. The low-frequency stimulation of all amygdaloid nuclei induced depressor reactions, while the high-frequency stimulation of the same areas induced an obvious pressure response. The pressure effect, however, was less obvious and of shorter duration as compared with the hypothalamic pressure responses. No correlation was found between electrical seizure discharges and blood pressure reactions to the low- and high-frequency stimulation. Mechanisms of reversal of vasomotor responses to stimulation of amygdala, diffuse organization of amygdaloid sympathoactivating mechanisms, and amygdaloid mechanisms of vasomotor regulation, are discussed.

A mathematical model for estimation of regulatory abilities of pial and intracerebral arteries was used for studying the pressure - radius relationships for arteries of various calibres in passive and active states. In passive state the arteries were found to be characterized by high elasticity and low tensile force. The radius of the artery depends mainly on the smooth muscle contractile force. The data obtained suggest that the wall structure of small pial and intracerebral arteries well correspond to their function: the control of the adequate and rapid cerebral blood flow.

In humorally isolated small intestine, the 10--20%--decrease in the perfusing blood volume against the background of augmented vascular resistance of the small intestine, induces different shifts of the latter's vascular capacitance. At the blockade of small intestine's beta--adrenoreceptors the decrease does not practically tell on the character of shifts in the intestine's resistance and capacitance while the blockade of alpha--adrenoreceptors abolishes the augmentation of these parameters.

Continuous recording of local blood flow in the cat cerebral cortex (the technique of electrochemical generation of hydrogen in brain tissue) revealed dynamic characteristics of autoregulation of the cerebral blood flow (CBF) during changes in the systemic arterial blood pressure. The autoregulation has a three-component character due to joint functioning of the mechanisms of myogenic, neurogenic and metabolic nature. The myogenic mechanism seems to protect the vascular bed of the brain from the impact of sharp changes in the intravascular pressure and is but indirectly involved in the CBF regulation, the latter being accomplished mainly by the hierarchically interacting nervous and metabolic mechanisms.

In acute experiments on cats using resistography and extracorporeal venous reservoir, responses of the small intestine's arterial and venous vessels were studied by means of successive pressor reflexes, electrical stimulation of the splanchnic nerve (1-80/sec) and i.a. administration of different doses of adrenaline (A) and noradrenaline (NA). The maximal constrictor responses of the vessels occurred mainly on the 10/sec stimulation; A induced mainly an increase in the perfusion pressure and venous outflow whereas NA induced chiefly an increase in the perfusion pressure and diminishing of the venous outflow. In pressor reflexes, low-frequency stimulation of the splanchnic nerve (2-5/sec) and i.a. administration of A, the venous vessels actualise a considerably greater part of the possible neurogenic constriction as compared to the arteries. The constrictor responses of the arteries in the pressor reflexes under study are equal to those on either left splanchnic nerve stimulation (1-2.5/sec) or i.a. administration of A or NA in doses lower than 0.5-1.0 mcg. The constrictor responses of the venous vessels in these conditions are equal to those on either left splanchnic nerve stimulation (3-8/sec) or i.a. administration of A in doses 0.5-1.0 mcg.

The activity of antidromically identified sympathetic preganglionic neurons (SPNs) located in the lateral horn of the L2--L3 spinal cord segments was recorded in anesthetized and immobilized cats. The localization of SPNs with tonic activity and the conduction velocities of their axons were revealed. Two groups of SPNs were shown which increased their firing rates either in cooling or heating of the abdominal skin. Some intermediate neurons possibly conducting thermal information to SPNs, were studied. The data obtained are considered within the limits of segmentary model of the vasomotor thermoregulatory reaction.

The blood flow in the lung lobe perfused under constant pressure was recorded with photoelectric drop recorder in acute closed-chest experiments in anesthetized dogs. Stimulation of supraoptic and lateral mamillary nuclei in most cases decreased flow rate and increased vascular resistance in perfused pulmonary lobe, while stimulation of sympatho-inhibitory area exerted opposite effect. Bilateral vagotomy and administration of atropin and inderal did not block the lesser circulation responses to the hypothalamic stimulation. However, phentolamine and bilateral ablation of stellate and upper thoracic ganglia eliminated chnages of blood flow and vascular resistance in the perfused lobe. The data obtained suggest that stimulation of some hypothalamic areas evoke obvious vasomotor responses in the lesser circulation and that these responses occur mainly through alpha-adrenergic sympathetic innervation of pulmonary vessels.

Responses of arterial blood pressure to low- and high-frequency stimulation of different structures of the limbic cortex and hypothalamus were studied in anesthetized and immobilized cats. The low-frequency (5 Hz) stimulation induced depressor reactions, the high-frequency (100 Hz) one-pressor responses. Both kinds of stimulation in the dorsal level of area 25 and of area 23 of the limbic cortex and of the anterior hypothalamus induced similar depressor responses, whereas the hypothalamic structures in the posterolateral region induced only pressor responses. The role of poly-effectory, sympatho-inhibitory and sympatho-activating neurons responsible for the observed three patterns of the blood pressure changes in low- and high-frequency stimulation of limbic cortex and hypothalamus, is discussed.

Supersound flowmetry revealed that the effect of heat (50 degrees C) involved an increase of the blood flow in skin vessels and its decrease in the vessels of small intestine and skeletal muscles. The blood flow resistance was diminished in skin vessels and increased in the vessels of small intestine and skeletal muscles. These shifts of the regional blood flow are due to the integral interaction of active and passive vascular responses. Specifics of the small intestine and skeletal muscle vessels' constrictory responses to hyperthermia suggest a difference in the mechanisms of their occurrence.

With the aid of thermometry and calorimetry, the role of the organism's heat degree for the vasomotor response of the ear skin was studied in the rabbit. The calorimetric temperature was constant (19-21 degrees C) throughout the experiment. The heat threshold varied from 86 cal/kg to 320 cal/kg, depending on the different initial heat degrees in the animal. The increase in the organism's heat degree is concluded to be the main mechanism for initiation of the heat loss responses.

The quantitative analysis of hemodynamic shifts during cardiovascular responses to stimulation of central neural structures, and recording of electric activity from the sympathetic fibers elucidate different links in the complex mechanism of the hemodynamic control. Monosynaptic connections of the sino-aortic zone with some structures of the bulbar level seem to contain relevant information on the blood pressure and the gas content. Differentiated modulated influences project from the cerebellum to the bulbar level, and complex interrelationships of local metabolic and central reflex mechanisms occur during acute hypoxic hypoxia.

In cats, during perfusion of the shank with a constant blood volume and in artificial changing of the venous pressure, the electric stimulation of the lumbal sympathetic chains and administration of noradrenaline in the perfusate were shown to be able to evoke both the constrictory and the dilatory responses of the capacitance vessels against the background of constriction of the resistance vessels. The 10--15 mm Hg venous pressure was optimal for the constrictory responses of the shank capacitance vessels. At the extreme levels of venous pressure (0;5 and 20;25 mm Hg), the relative weight of dilatory responses of the capacitance vessels was increased in the sum total of responses to the used adrenergic effects.

The alterations of blood supply in restricted regions of the abdominal skin and the external oblique muscle were studied in anesthetized cats with photoplethysmographic technique. Local cooling of the abdominal skin decreased blood supply in skin and muscle whereas heating exerted an opposite effect. Vasomotor responses of skin and muscle abdominal blood vessels to somatic and visceral afferent fibre stimulation and injections of alpha- and beta-adrenergic agonists were mostly active in character. The abdominal wall vasomotor responses seem to be a proper experimental model for studying segmental vasomotor control.

In anesthetized cats, the cold block or coagulation of intermediate zones of the bulbar ventro-lateral surface (BVLS) resulted in profound decrease of the blood pressure (BP) level. The descending tonic activation of spinal vasomotor mechanism in formed by spontaneous discharges of antidromically identified output sympatho-activating neurons with mean firing rate about 14.4/sec. After coagulation of the intermediate zone, pressure reflexes of the BP and late somato-sympathetic response in white rami disappear whereas the spino--bulbo--spinal somato--somatic reflex remains unchanged. The reflex discharges of single sympatho--activating neurons were within the time limits of the late somato--sympathetic response and followed by the silent period. The preferable inhibition of the long-latency white rami discharges elicited by BVLS stimulation arise 200-250 msec after R-wave of the ECG. The inhibition of long-latency discharges was observed during the increase of the BP level induced with vasoconstrictor drugs. The intermediate zone structures of BVLS seem to play the key role in supporting of the BP level and organization of pressure reflexes. These structures are suggested to be the actual elements of the bulbar vasomotor center.

The changes of cerebral blood flow registered by means of flowmeter in the common carotid artery were investigated during fast raise and drop of arterial blood pressure in acute experiments on anesthetized cats. Both the raise and drop of arterial pressure resulted in fast autoregulatory changes of cerebral blood flow occurring even after resection of cervical sympathetic ganglia. The alpha-adrenergic blockade abolished the fast autoregulatory phase during raise of the arterial pressure. These findings sugget participation of noradrenergic mechanisms in reaction to acute hypertension.

A correlation was found between the initial relative thickness of vascular wall and the extent of vasoconstriction in response to standard stimulation of sympathetic strings. The distribution of vessels within the wall was comprised in mathematical model which estimated interrelationships among three variables: pressure perfusate expenditure and a conventional dose of vasoconstricting agent. The model revealed that intense vasoconstrictory responses entailed a decrease in the number of functioning vessels. When perfusing the rat hindlimbs with a constant expenditure in maximal vasoconstriction, the number of functioning microvessels decreased by 46 +/- 11.9%.

In isolated preparations of the rabbit ear artery, the contractile response to a single electrical stimulus and its latency were studied at different degrees of stretching. Contractile responses were compared in direct and indirect stimulations of the vessel's smooth muscle at different temporal interrelationships between the stimulus and the stretching process. The contractile response was found to augment in indirect stimulation within a certain stretch area of the vascular ring whereas its latency was found to shorten. The direct stimulation of the desympathised vessel left latency the same whereas the contractile response started to diminish at a lesser stretching. The comparison of contractile responses of the artery's smooth muscle in indirect and direct stimulations suggests that, with reduction of neuro--muscular distances, an automatic increase of adrenergic effects on the vascular wall occurs. The significance of this phenomenon for vascular tone control is discussed.

Redundant afferentation from reflexogenic zones of the lung and skeletal muscles alters effects of electric stimulation of the midbrain reticular formation and posterior hypothalamic nucleus in the cat due to readjustment of the cortico--subcortical interrelationships and to an increase in the excitability of the brain structures. The data suggest that the functional activity of the vasomotor center depends on the character of afferentation from different reflexogenic zones.

Perfusion of the small intestine of anesthetized cats with a solution having excessive CO2 and H+ concentration (pCO2 60 mm Hg; pH; 7.2; [HCO3-] 25 MM) produced a threshold reflex increase in the blood pressure. The subsequent increase of pCO2 to 380 mm Hg and decrease of pH to 6.4 evoked a gradual raise of the blood pressure (8.0+/-0.6 mm Hg) followed by the sharp increase of pressor reflexes amplitude within the range of pH 6.4--6.1. Tissue receptors were found to be essentially sensitive to solutions imitating metabolic acidosis (decrease of [HCO3-] within the physiological range of pH changes (pH 7.1--6.8). Solutions with pH 6.4--6.1 imitating respiratory acidosis (increase of pCO2) were more effective than those imitating metabolic acidosis. The possible role of interstitial pH changes in responses of the tissue chemoreceptors to CO2, is discussed.

Functional stability of the cerebral circulation system seems to be based on the active mechanisms and on those stemming from specifics of the biophysical structure of the system under study. This latter parameter has some relevant criteria for its quantitative estimation. Analysis of common data on various effects upon cerebral vessels shows an essential difference between the functional stability and the idea of "autoregulation of the cerebral circulation". The data obtained suggest that the essential part of the mechanism for active responses of cerebral vessels which maintains the functional stability of this portion of the vascular system, consists of a neurogenic component involving central nervous structures localized, for instance, in the medulla oblongata.

In cats and dogs, cardiovascular responses were studied during stimulation of afferents, intraspinal pathways, after changes in composition of interneuronal media, 3rd ventricle's and spinal fluid. The longer hemodynamic responses as compared with the reflex and humoral those, preservation in conditions of spinal shock, their increased markedness together with weakening of the reflex regulation, their interrelationship with the reflex effects, their differentiation associated with the type of affecting drugs and with morpho-functional features of the central mechanisms of regulation and, finally, their integration with the reflex and hemato-encephalic influences in determination of the final hemodynamic effect,--all these constituted the six revealed features. Possible controlling role of the fluid effects is discussed.