Reflex vascular responses to changes in left ventricular pressures, heart rate and inotropic state in dogs.

Dogs were anaesthetized with chloralose, artificially ventilated and the chests widely opened. Left ventricular mechanoreceptors, including those in or near the coronary arteries, were stimulated by changing the pressure in the aortic root. The pressures distending the left atrium and the aortic and carotid baroreceptors were controlled. Reflex vascular responses were assessed from changes in perfusion pressures to a hind limb and to the rest of the systemic circulation, which were perfused independently at constant flows. Physiological increases in peak left ventricular and coronary arterial pressures resulted in vasodilatation in both regions. These responses were not influenced by changes in the heart rate. Stimulation of the left cardiac sympathetic nerves resulted in increases in peak ventricular pressure and in the maximal rate of change of pressure (dP/dtmax). This also resulted in increases in perfusion pressures (vasoconstriction) at all levels of peak ventricular pressure although there was little effect on the responses to changes in ventricular pressure. Sympathetic stimulation had little effect on the relationship between perfusion pressures and aortic root pressure. Increases in ventricular filling also resulted in vasoconstriction at all levels of peak ventricular pressure. Increases in filling, however, did not affect the relationship between either perfusion pressure and aortic root pressure. Conversely, decreases in left ventricular filling, by bypassing some of the left atrial blood, resulted in vasodilatation at all levels of peak ventricular pressures but had no effect on the perfusion pressures at any aortic root pressure. The combination of sympathetic stimulation with decreased ventricular filling resulted in little effect on perfusion pressures or on their responses to changes in either aortic root or ventricular systolic pressures. We conclude that the vascular responses to stimulation of left ventricular mechanoreceptors are not enhanced by sympathetic stimulation, decreases in ventricular filling or the combination of the two. The apparent effects of each of these interventions alone on the relationships between perfusion pressures and ventricular, but not aortic root, pressure, could be explained if the receptors responsible were sensitive more to changes in aortic root and coronary arterial pressures than to pressure changes in the ventricle itself.     

Left ventricular mechanoreceptors: a haemodynamic study

1. To study the function of the left ventricular mechanoreceptors, a working left ventricle preparation was devised in dogs which permitted control of pressure and flow of the isolated perfused coronary circulation and of the flow of the isolated, separately perfused systemic circulation. The systemic circulation was perfused at a constant rate so that changes in systemic pressure reflected changes in systemic resistance.2. Increases in myocardial contractility produced by injection of catecholamines into the isolated, perfused coronary circulation produced a fall in the pressure (resistance) of the isolated, separately perfused (at a constant rate) systemic circulation.3. Completeness of isolation of the coronary and systemic circulations was shown by the marked difference in appearance times between the reflex hypotensive responses from catecholamine injections into the isolated coronary circulation and the direct hypertensive response from a similar injection when the circulations were connected as well as by the marked difference between the pressure pulses recorded simultaneously on both sides of the aortic balloon separating the two circulations.4. Myocardial beta receptor blockade produced by injection of propranolol into the isolated coronary circulation abolished or attenuated the changes in left ventricular myocardial contractility as well as the subsequent hypotensive responses following the similar injection of catecholamines.5. Electrical stimulation of a sympathetic nerve innervating the heart resulted in increases in left ventricular myocardial contractility and subsequent systemic hypotensive responses indistinguishable from those following injection of catecholamines.6. That distortion of the mechano- or stretch receptors in the left ventricular myocardium was the cause of the hypotensive responses was demonstrated by increasing left ventricular myocardial contractility by mechanically obstructing the left ventricular outflow which produced hypotensive responses similar to those following the injection of catecholamines or nerve stimulation.7. Bilateral high cervical vagotomy abolished the hypotensive responses following injection of catecholamines into the isolated coronary circulation or following left ventricular outflow obstruction in all but one instance, indicating the importance of vagal fibres to the afferent arm of the reflex.8. It is suggested that the left ventricular mechanoreceptors function normally to reduce the peripheral resistance in order to prepare the systemic circulation to receive the left ventricular output and, especially during exercise, to prepare the systemic circulation to receive the augmented cardiac output with a minimum alteration in the systemic blood pressure and to distribute this augmented output preferentially to the skeletal muscles.     

Coronary vascular and myocardial responses to carotid body stimulation in the dog.

Coronary vascular and myocardial responses to selective hypoxic and/or hypercapnic carotid chemoreceptor stimulation were investigated in constantly ventilated, pentobarbital or urethan-chloralose anesthetized dogs. Bilaterally isolated carotid chemoreceptors were perfused with autologous blood of varying O2 and CO2 tensions via an extracorporeal lung circuit. Systemic gas tensions were unchanged. Effects of carotid chemoreceptor stimulation on coronary vascular resistance, left ventricular dP/dt, and strain-gauge arch output were studied at natural coronary blood flow with the chest closed and during constant-flow perfusion of the left common coronary artery with the chest open. Carotid chemoreceptor stimulation slightly increased left ventricular dP/dt and slightly decreased the strain-gauge arch output, while markedly increasing systemic pressure. Coronary blood flow increased; however, coronary vascular resistance wa.as not affected. These studies show that local carotid body stimulation increases coronary blood flow but has little effect on the myocardium. The increase in coronary blood flow results mainly from an increase in systemic arterial pressure. Thus these data provide little evidence for increased sympathetic activity of the heart during local stimulation of the carotid chemoreceptors with hypoxic and hypercapnic blood.     

Coronary flow and left ventricular pressure during diastole in the anaesthetized dog.

There is controversy about the effect of left ventricular pressure on resistance of the intramyocardial coronary vessels. In anaesthetized dogs the effect of left ventricular pressure on coronary flow during diastole was studied using an extracorporeal circulation and allowing the heart to contract and relax isovolumically. At constant coronary perfusion pressure of about 45 mmHg with maximal coronary vasodilatation, produced by dipyridamole, increases in diastolic left ventricular pressure to 22 mmHg, producing a volume of 50 ml, did not affect diastolic coronary flow. It is suggested that in the intact animal over the physiological range of left ventricular diastolic pressure the resistance in the coronary vessels is not affected.     

Patient-Specific Modeling of Blood Flow and Pressure in Human Coronary Arteries

Coronary flow is different from the flow in other parts of the arterial system because it is influenced by the contraction and relaxation of the heart. To model coronary flow realistically, the compressive force of the heart acting on the coronary vessels needs to be included. In this study, we developed a method that predicts coronary flow and pressure of three-dimensional epicardial coronary arteries by considering models of the heart and arterial system and the interactions between the two models. For each coronary outlet, a lumped parameter coronary vascular bed model was assigned to represent the impedance of the downstream coronary vascular networks absent in the computational domain. The intramyocardial pressure was represented with either the left or right ventricular pressure depending on the location of the coronary arteries. The left and right ventricular pressure were solved from the lumped parameter heart models coupled to a closed loop system comprising a three-dimensional model of the aorta, three-element Windkessel models of the rest of the systemic circulation and the pulmonary circulation, and lumped parameter models for the left and right sides of the heart. The computed coronary flow and pressure and the aortic flow and pressure waveforms were realistic as compared to literature data.     

Bimodality of cardiac vagal afferent C-fibres in the rat

Vagal afferent C-fibres from the heart constitute an important input to the neurogenic cardiovascular regulation. These fibres respond to altered cardiac filling pressures and to chemical stimuli. In rats, we tested whether cardiac vagal afferent C-fibres react exclusively to one stimulus (chemical or mechanical) or whether the fibres are bimodal, i.e. responsive to either kind of stimulus. As a mechanical stimulus, an indwelling balloon was inflated in the aorta to increase left ventricular end-diastolic pressure. The serotonin 5HT(3) receptor agonist phenylbiguanide was injected into the pericardial sac as a chemical stimulus. An increase of fibre activity by more than two standard deviations compared with control was considered a response to a stimulus. Most fibres (42 out of 57) responded to both stimuli and were categorized as bimodal, 9 fibres were solely mechanosensitive and 6 were solely chemosensitive. Hence, the majority of cardiac vagal C-fibres are likely to be bimodal, responding to both cardiac filling pressure and serotonin 5HT(3) receptor stimulation. Our results emphasize the potential role of endogenous mediators in the afferent limb of cardiac reflexes.     

Cutaneous Mechanical Stimulation Regulates Ovarian Blood Flow via Activation of Spinal and Supraspinal Reflex Pathways in Anesthetized Rats

The reflex effects of noxious mechanical stimulation of a hindpaw or abdominal skin on ovarian blood flow, and the reflex pathways involved in those responses were examined in anesthetized rats. Blood flow in the left ovary was measured using a laser Doppler flowmeter, and the activity of the left ovarian sympathetic nerve and mean arterial pressure (MAP) of the common carotid artery were recorded. Stimulation of the left or right hindpaw for 30 s produced marked increases in ovarian sympathetic nerve activity and MAP. Ovarian blood flow slightly decreased during the stimulation and then slightly increased after the stimulation. After the left ovarian sympathetic nerves were severed, the same stimulus produced a remarkable monophasic increase in ovarian blood flow that was explained by passive vasodilation due to a marked increase in MAP. After spinal transection at the third thoracic (T3) level, the responses of MAP, ovarian sympathetic nerve activity, and ovarian blood flow to hindpaw stimulation were nearly abolished. Stimulation of the abdomen at the right or left side for 30 s produced slight increases in ovarian sympathetic nerve activity and MAP. Ovarian blood flow slightly decreased during the stimulation and then slightly increased after the stimulation. After the ovarian sympathetic nerves were severed, the response of the ovarian blood flow changed to a monophasic increase due to an increase in MAP. After spinal transection, stimulation of the left abdomen produced a moderate increase in MAP, a remarkable increase in ovarian sympathetic nerve activity and a slight decrease in ovarian blood flow during the stimulation. In contrast, stimulation of the right abdomen produced a smaller response in ovarian sympathetic nerve activity during the stimulation while it increased the MAP to a similar degree. Ovarian blood flow slightly increased after the end of stimulation, which was explained as passive vasodilation due to the increase in MAP. In conclusion, stimulation of somatic afferents affects ovarian blood flow by inducing changes in ovarian sympathetic nerve activities and blood pressure. When stimulation was applied to a hindpaw whose segment of afferent input is far from the segment of the ovarian sympathetic nerves, it took a supraspinal reflex pathway. However, when stimulation was applied to the abdomen whose spinal segment of the afferent is close to the segment of the ovarian sympathetic nerve output, there are spinal segmental reflex pathways. The present results demonstrate that spinal reflexes depend on the laterality of the stimulus, while supraspinal reflexes do not depend on the laterality of the stimulus.     

Comparison between isoprenaline infusions and bolus injections to assess beta-adrenoceptor function in man, with special reference to cardiac contractility and the influence of autonomic reflexes.

The present study was performed to characterize cardiovascular responses to isoprenaline and the influence of autonomic reflexes on these responses. Nine healthy volunteers received infusions and bolus injections of isoprenaline before and after 'autonomic blockade' produced by intravenous atropine 0.04 mg kg-1 and clonidine 300 micrograms. Heart rate, blood pressures, systolic time intervals and various echocardiographic measures of cardiac contractility were registered. No significant differences in responsiveness to isoprenaline were seen when infusions were repeated on the same day without 'autonomic blockade'. After 'blockade', delta responses at 1 nmol l-1 isoprenaline (infusions) were increased for diastolic blood pressure and decreased for systolic blood pressure and stroke volume. Bolus injections of 2 micrograms isoprenaline caused enhanced delta responses after 'autonomic blockade' of diastolic blood pressure, left ventricular diameter in systole, ventricular circumferential fibre shortening, mean posterior wall velocity (Vmean PW), stroke volume, systemic vascular resistance, electromechanical systole (QS2) and pre-ejection period. Systolic blood pressure decreased, in contrast to a small increase without 'blockade'. These findings are explained by differences in haemodynamic effects of isoprenaline and by the dependence of responses on reflexes when isoprenaline is administered in different ways. When heart rate was increased by bolus doses of atropine, in the presence of beta-blockade (propranolol), pre-ejection period and left ventricular diameter in systole were unaffected, and Vmean PW and ventricular circumferential fibre shortening showed only small increases (compared with alterations induced by isoprenaline). However, left ventricular ejection time, QS2 and ejection time (by echocardiography), were markedly dependent on heart rate alterations. Thus, pre-ejection period, left ventricular diameter in systole Vmean PW and ventricular circumferential fibre shortening are parameters which can be useful in order to evaluate cardiac beta-adrenoceptor sensitivity in vivo in man.     

Central interaction between the baroreceptor reflexes from the carotid sinus and aortic arch.

The cardiovascular response to combined stimulation of the aortic nerve (AN) and carotid sinus nerve (CSN) with trains of electrical stimuli was studied in dogs under morphine-chloralose anesthesia. Combined stimulation of both nerves ipsilaterally resulted in systemic arterial depressor responses and cardiac slowing that were 59% and 77% greater (P less than 0.05) than the respective sum of the responses to separate stimulation of these nerves. The depressor response to combined stimulation of these nerves contralaterally was not different (P greater than 0.05) from the sum of the separate responses. However, cardiac slowing to contralateral stimulation of the nerves remained 43% greater (P less than 0.05) than the sum of the individual responses. The results suggest that an interaction between the aortic and carotid baroreceptor reflexes occurs centrally, which causes a greater than additive effect on the autonomic output. The degree of interaction between the reflexes did not change as the delay between the stimulus trains was varied over an interval of 0 and 100 ms. At intervals greater than 100 ms the reflex responses were additive.     

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

The present study was designed to investigate the effect of progesterone on the coronary circulation and to determine the mechanisms involved. In pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous infusion of progesterone at constant heart rate and arterial blood pressure were assessed using an electromagnetic flowmeter. In 14 pigs, infusion of 1 mg h(-1) of progesterone caused an increase in coronary blood flow without affecting left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In a further four pigs, this vasodilatory coronary effect was enhanced by graded increases in the dose of the hormone of between 1, 2 and 3 mg h(-1). The mechanisms of the above response were studied in the 14 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the coronary vasodilatation caused by progesterone. In the remaining eight pigs, this response was abolished by intracoronary injection of N(omega)-nitro-L-arginine methyl ester (L-NAME) even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L-NAME with continuous intravenous infusion of papaverine. The present study showed that intravenous infusion of progesterone primarily caused coronary vasodilatation. The mechanism of this response was shown to involve the endothelial release of nitric oxide.     

Hemodynamic and pressure-volume responses to continuous and pulsatile ventricular assist in an adult mock circulation

This study investigated the hemodynamic and left ventricular (LV) pressure-volume loop responses to continuous versus pulsatile assist techniques at 50% and 100% bypass flow rates during simulated ventricular pathophysiologic states (normal, failing, recovery) with Starling response behavior in an adult mock circulation. The rationale for this approach was the desire to conduct a preliminary investigation in a well controlled environment that cannot be as easily produced in an animal model or clinical setting. Continuous and pulsatile flow ventricular assist devices (VADs) were connected to ventricular apical and aortic root return cannulae. The mock circulation was instrumented with a pressure-volume conductance catheter for simultaneous measurement of aortic root pressure and LV pressure and volume; a left atrial pressure catheter; a distal aortic pressure catheter; and aortic root, aortic distal, VAD output, and coronary flow probes. Filling pressures (mean left atrial and LV end diastolic) were reduced with each assist technique; continuous assist reduced filling pressures by 50% more than pulsatile. This reduction, however, was at the expense of a higher mean distal aortic pressure and lower diastolic to systolic coronary artery flow ratio. At full bypass flow (100%) for both assist devices, there was a pronounced effect on hemodynamic parameters, whereas the lesser bypass flow (50%) had only a slight influence. Hemodynamic responses to continuous and pulsatile assist during simulated heart failure differed from normal and recovery states. These findings suggest the potential for differences in endocardial perfusion between assist techniques that may warrant further investigation in an in vivo model, the need for controlling the amount of bypass flow, and the importance in considering the choice of in vivo model.     

Force-sensitive mechanoreceptors of the dactyl of the crab: single-unit responses during walking and evaluation of function

The activities of individual force-sensitive mechanoreceptors of the dactyl (terminal leg segment) of the crab, Carcinus maenas, have been recorded during free walking. These receptors have also been mechanically and electrically stimulated in freely moving animals to directly evaluate their function in locomotion. All force-sensitive mechanoreceptors fired during the stance phase of walking and were silent during swing. Receptor discharges showed regular phase relationships to bursts in motor neurons of leg muscles. Crabs walk laterally and use the legs of one side either in trailing to actively push the animal to the opposite side, or in leading, to less forcefully pull the animal in that direction. Individual force-sensitive mechanoreceptors differed in their patterns of activity during trailing or leading according to their location on the dactyl. Units of proximal receptors fired more vigorously when used in trailing than in leading. Discharges in trailing were also increased by loading of the animal. In contrast, distal receptors near the dactyl tip fired equally intensely during walking in either direction. Proximal receptors thus encode forces and loads applied to the leg. Distal receptors do not encode loads but can signal leg contact and, potentially, exteroceptive vibrations. Sensory stimulation of force-sensitive mechanoreceptors was produced during walking by a device that imposed continuous mechanical bending of the dactyl and by electrical stimulation of dactyl nerves. Intra- and inter-segmental reflexes were evaluated by myographic recordings from leg muscles. Continuous mechanical deformation of the dactyl increased the activity of the levator and decreased firing in the depressor muscles of the homonymous leg during walking. The same stimulus produced enhanced activity in depressor muscles of adjacent legs. The latter effect was not due to simple mechanical coupling resulting from reflexes in the stimulated leg. These reflexes can function to limit forces applied to a leg and provide compensatory adjustments in other legs. Brief low-threshold electrical stimuli applied to nerves in which the activities of force-sensitive mechanoreceptors were recorded produced reflex effects similar to those obtained by mechanical stimulation. These stimuli also reset the rhythm of motor neuron bursting in both homonymous and adjacent legs during walking. These studies confirm the importance of force-sensitive mechanoreceptors in adapting walking patterns and in determining leg coordination in locomotion.     

The effect of amino acids on unconditioned interoceptive reflexes

Summary The aim of this work was the study of the effect of amino acids on the unconditioned interoceptive reflexes. The work was conducted on fasting cats and on those which were fed in condition of urethane anesthesia. Neutralized solutions of glutamic acid, cysteine and alanine were injected intravenously in the 1 : 10^–3 concentration. The author studied the changes of the reflex reactions in response to the stimulation of duodenal mechanoreceptors, the chembreceptors of the perfused section of the small intestine, the baroreceptors of carotid sinus and in response to the electric stimulation of the central end of the femoral nerve. After the intravenous administration of amino acids to fasting animals a change of the blood pressure pressor reactions into depressor was noted, while in animals which were fed the depressor reactions changed into pressor. The pressor reflex to stimulation of the femoral nerve was depressed both in fasting cats and in those which were fed. In stimulation of the baroreceptors of carotid sinus in these conditions the reflexes did not follow any definite laws.Reactions in response to the stimulation of the chemoreceptors of the perfused portion of intestine did not change. Thus, the intravenous administration of amino acids has a definite effect on the character of the reflexes, mainly by changing the condition of the peripheral part of the reflex arc.Evidently, the change in the metabolic processes occurring in the receptive zones and the impulsation which is transmitted from the zone to the central nervous system are decisive in the mechanism of interoceptive reflexes.Presented by Active Member of the AMN SSSR V. N. Chernigovskii     

Modification of the reflex response to stimulation of carotid sinus baroreceptors during and following stimulation of the hypothalamic defence area in the cat

1. The effects of stimulation of the hypothalamic defence area on carotid sinus baroreceptor reflexes have been investigated by examining the cardiovascular responses to a 15 sec period of increased pressure within the vascularly isolated carotid sinus before, during, and immediately following a 25 sec period of hypothalamic stimulation.2. Identification of the hypothalamic defence area was based on the occurence of atropine-sensitive muscle vasodilatation. Electrode positions were confirmed by histological examination.3. During hypothalamic stimulation the reflex fall in blood pressure resulting from a rise in sinus pressure was found to be undiminished whether sinus pressure was raised at the onset or at the 10th sec of hypothalamic stimulation.4. By contrast, in at least half the cats in which a reflex bradycardia could be evoked from the sinus, this bradycardia was largely if not completely suppressed during hypothalamic stimulation. This suppression of reflex bradycardia occurred when sinus pressure was raised at the onset as well as at the 10th sec of stimulation.5. During the first 5 sec after hypothalamic stimulation the hypotensive response to an increase in carotid sinus pressure was much reduced; on the other hand the reduction in heart rate was exaggerated, sometimes to a very marked degree.6. The results suggest that stimulation of the hypothalamic defence area can modify baroreceptor reflexes and that this modification can include selective alterations in the various components of the reflex response.     

Action potentials from ventricular mechanoreceptors stimulated by occlusion of the coronary sinus in the dog

1. In experiments to determine the type of intra-cardiac receptors which cause the coronary sinus occlusion reflex, recordings were made from sixty-nine single and small multi-fibre preparations of cardiac vagal afferents in open-chest anaesthetized dogs.2. Thirty-two fibres were stimulated by occlusion of the coronary sinus outflow through an indwelling Morawitz cannula. No receptors were stimulated during occlusions at peak systolic coronary venous pressures below the threshold for reflex cardiovascular depression. At higher pressures, fibre recruitment and further increases in stimulated discharge were demonstrated.3. The afferent endings of twenty-nine of these fibres were mechanically localized to the epicardium and myocardium of the left ventricle. Three were in the right ventricle. Seventeen single fibres discharged spontaneously at an average of 0.9 impulses/sec. There was cardiac modulation of both resting and stimulated discharge, with most action potentials in systole. Seven of eight fibres conducted at less than 1.0 m/sec.4. These ventricular receptors and a further twenty-two otherwise like them but not stimulated by occlusions were designated epi-myocardial receptors.5. 73% of receptors were stimulated by intrapericardial nicotine (50-100 mug). Presumptively superficial receptors were more sensitive to this stimulus.6. Epi-myocardial receptors were stimulated by intravenous or intracoronary catecholamines, by electrical stimulation of cardiac sympathetic nerves, and by eliciting the carotid sinus occlusion reflex. Aortic occlusion stimulated 66% of fibres tested, but was a less effective stimulus. After all these stimuli, there was a systolic modulation of discharge in more than 70% of fibres.7. It was concluded that the epi-myocardial receptors are similar to those previously shown to cause the epicardial chemoreflex, and to participate in the coronary chemoreflex. It is suggested that they are responsive to systolic mechanical changes which are accentuated by catecholamines. Their possible effectiveness in other cardiac reflexes and in initiating circulatory changes at the beginning of exercise and the vasovagal syndrome is discussed.     

The selective effect of some chemical stimulants on the reflexes from chemoreceptors

Summary Short-term experiments were performed on cats under urethan anesthesia. The effect of streptomycin administered parenterally on the reflexes from the pericardial chemoreceptors and mechanoreceptors was studied. Intravenous injection of streptomycin in the dose of 250,000–400,000 units and in intramuscular injection of 70,000–127,000 units completely depresses or considerably inhibits the reflexes from the pericardial chemoreceptors caused by nicotine. However, in the majority of experiments no depression of reflexes appearing in stimulation of pericardial mechanoreceptors was noted in similar experimental conditions. At times only an insignificant decrease of these reflexes was revealed.Presented by Active Member Acad. Med. Sci. USSR, V. N. Chernigovskii     

Absence of reflex vascular responses from the intrapulmonary circulation in anaesthetised dogs

The aim of this investigation was to determine whether reflex cardiovascular responses were obtained to localised distension of the intrapulmonary arterial and venous circulations in a preparation in which the stimuli to other major reflexogenic areas were controlled and the lung was shown to possess reflex activity. Dogs were anaesthetised with -chloralose, artificially ventilated, the chests widely opened and a cardiopulmonary bypass established. The intrapulmonary region of the left lung was isolated and perfused through the left pulmonary artery and drained through cannulae in the left pulmonary veins via a Starling resistance. Intrapulmonary arterial and venous pressures were controlled by the rate of inflow of blood and the pressure applied to the Starling resistance. Pressures to the carotid, aortic and coronary baroreceptors and heart chambers were controlled. Responses of vascular resistance were assessed from changes in perfusion pressures to a vascularly isolated hind limb and to the remainder of the subdiaphragmatic circulation (flows constant). The reactivity of the preparation was demonstrated by observing decreases in vascular resistance to large step changes in carotid sinus pressure (systemic vascular resistance decreased by -40 +/- 5%), chemical stimulation of lung receptors by injection into the pulmonary circulation of veratridine or capsaicin (resistance decreased by -32 +/- 4%) and, in the four dogs tested, increasing pulmonary stroke volume to 450 ml (resistance decreased by -24 +/- 6%). However, despite this evidence that the lung was innervated, increases in intrapulmonary arterial pressure from 14 +/- 1 to 43 +/- 3 mmHg or in intrapulmonary venous pressure from 5 +/- 2 to 34 +/- 2 mmHg or both did not result in any consistent changes in systemic or limb vascular resistances. In two animals tested, however, there were marked decreases in efferent phrenic nerve activity. These results indicate that increases in pressure confined to the intrapulmonary arterial and venous circulations do not cause consistent reflex vascular responses, even though the preparation was shown to be reflexly active and the lung was shown to be innervated.     

Characteristics of adaptation of cardiovascular reflexes in old animals

Summary Experiments were made on 96 old and young rabbits and 22 cats of various ages to study the age peculiarities of adaptation of cardiovascular reflexes in prolonged stimulation of different extero- and interoceptive fields, as well as of the sensory nerves. In old animals the weakening of reflexes in prolonged stimulation of the rectum, the tibial nerve, the chemo- and mechanoreceptors of the carotid sinus and the aortal nerve had a faster onset. In such animals, prolonged stimulation may produce deep inhibition of the central functions followed by death or failure of the inhibitory process and a stable change in the blood pressure.(Presented by Academician V. N. Chernigovskii) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 60, No. 8, pp. 32–36, August, 1965     

Left ventricular inotropic and peripheral vasomotor responses from independent changes in pressure in the carotid sinuses and cerebral arteries in anaesthetized dogs

1. The pressure perfusing the isolated carotid sinuses and the pressure perfusing the cerebral circulation were changed independently, and the resulting inotropic responses in the left ventricle and peripheral vasomotor responses were determined.2. Inotropic responses were assessed by measuring changes in the maximum rate of change of left ventricular pressure (dP/dt max) with heart rate and mean aortic pressure held constant. Vascular resistance changes were usually assessed by perfusing the descending thoracic aorta at constant flow and measuring changes in perfusion pressure.3. Decreases in carotid sinus pressure over the baroreceptor sensitivity range resulted in a 45% increase in dP/dt max and a 59% increase in vascular resistance.4. Unless arterial oxygen tension was abnormally low, lowering cerebral perfusion pressure to 50 mm Hg resulted in little or no inotropic and vasomotor responses. In the presence of hypoxaemia (P(a,O2) < 60 mm Hg), lowering cerebral perfusion pressure to below about 80 mm Hg resulted in marked responses.5. These experiments suggest that, unless arterial oxygen tension is abnormally low, the carotid sinus reflex and not cerebral hypotension is important in the control of the inotropic state of the heart and of vasomotor activity. With hypoxaemia, responses from cerebral hypotension may also be important.