Effects of graded pulsatile pressure on the reflex vasomotor responses elicited by changes of mean pressure in the perfused carotid sinus-aortic arch regions of the dog

1. In the anaesthetized dog, the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. We have confirmed our previous observations that under steadystate conditions the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in carotid sinus pulse pressure, whereas those evoked by changes of mean aortic arch pressure are only weakly affected by modifications of aortic pulse pressure.3. When the carotid sinus and aortic arch regions are perfused in combination at constant pulse frequency (110 c/min), the relationship between mean carotid sinus-aortic arch pressure and systemic arterial perfusion pressure is dependent on the size of the pulse pressure.4. Increasing the pulse pressure alters the curve relating the mean carotid sinus-aortic arch pressure to systemic arterial perfusion pressure in such a way that the perfusion pressure is lower at a given carotid sinus-aortic arch pressure within the range 80-150 mm Hg. The larger the pulse pressure, up to about 60 mm Hg, the greater the fall in systemic arterial perfusion pressure. Above a mean carotid sinus-aortic arch pressure of about 150 mm Hg, alterations of pulse pressure have little effect.5. There is a family of curves representing the relation between mean carotid sinus-aortic arch pressure and systemic vascular resistance, depending on the pulse pressure.     

The effects of changes of extramural, `intrathoracic', pressure on aortic arch baroreceptors

1. The isolated aortic arch was perfused by a method enabling the mean pressure, pulse pressure and pulse frequency to be varied independently. The preparation was also subjected to phasic and non-phasic changes of extramural pressure.2. The aortic arch baroreceptor impulse activity in single or few-fibre preparations was increased by raising the intra-aortic pressure and by applying a negative extramural pressure at constant intra-aortic pressure.3. Curves relating impulse frequency and negative extramural pressure were similar to those relating impulse frequency to intra-aortic pressure. The effective stimulus to the aortic arch baroreceptors is the transmural pressure resulting from the algebraic difference of the intra-aortic and extramural pressures.4. Rhythmical alterations in extramural pressure caused phasic changes in baroreceptor impulse activity. As the pressure became more negative, the impulse frequency increased and other baroreceptors were recruited.5. During pulsatile perfusion of the aortic arch the maximum impulse activity occurred when the negative phase of extramural pressure coincided with the systolic phase of the perfusion pressure.6. These findings are discussed in relation to the effects of changes of intrathoracic pressure on aortic baroreceptor activity in vivo     

The effects of altering mean pressure, pulse pressure and pulse frequency on the impulse activity in baroreceptor fibres from the aortic arch and right subclavian artery in the rabbit

1. A method is described for perfusing an isolated preparation of the rabbit aortic arch with independently controlled mean pressure, pulse pressure and pulse frequency.

2. Recordings made from single or few-fibre preparations from the aortic arch and right subclavian baroreceptor regions show that the number of impulses per second or per cycle in a single fibre is the same during pulsatile perfusion as during non-pulsatile perfusion if the pressure is above the threshold pressure to non-pulsatile perfusion during all phases of the pressure cycle.

3. In multi-fibre recordings the total number of impulses is greater during pulsatile perfusion than during non-pulsatile perfusion due largely to recruitment of fibres during systole.

4. The relationship between instantaneous impulse frequency and aortic arch pressure during one pressure cycle forms an elliptiform curve.

5. Increasing the pulse pressure increases the ellipse and causes additional recruitment of other fibres during systole, thus augmenting the total impulse activity.

6. Increasing the pulse frequency reduces the number of impulses per cycle for single fibres but produces a small increase in the total impulse frequency in one second period due to recruitment.

7. Increasing the rate of change of pressure by increasing the pulse pressure or pulse frequency produced a small reduction or no change of the threshold pressure. Similarly the `cut off' pressure was elevated in some fibres.

8. At low initial mean pressures, an increment of pressure, at constant pulse pressure and pulse frequency, increases the total impulse activity by increasing the frequency of impulses in single fibres already active during systole and diastole and by additional recruitment of other fibres. At higher mean pressures there is little increase in impulse activity as the maximum frequency of fibres is attained or superseded and there is little recruitment.

     

Interplay among carotid sinus, cardiopulmonary, and carotid body reflexes in dogs.

Interactions among vascular reflexes evoked from carotid sinuses, carotid bodies, and cardiopulmonary region were examined in anesthetized, atropinized, and respired dogs with aortic nerves cut. The carotid sinuses were perfused at 220, 150, and 40-50 mmHg; the chemoreceptors were stimulated by perfusion with hypoxic hypercapnic blood. Cardiopulmonary vasomotor inhibition was interrupted by vagal cold block. Measurements were made of arterial blood pressure and of kidney and hindlimb vascular resistance. At sinus pressures less than 170-160 mmHg, cardiopulmonary vasomotor inhibition increased with increase in blood volume. At high sinus pressure, interruption of this augmented cardiopulmonary inhibition was as ineffective in changing vascular resistance as interruption of the lesser inhibition present during normovolemia. Chemoreceptor stimulation increased the response to vagal block at intermediate but not at high or low sinus pressure. The studies demonstrate the dominant role of the carotid sinus reflex when the three systems interact and the ineffectiveness of chemoreceptor stimulation when carotid or cardiopulmonary inhibition is maximal.     

Inotropic responses of the left ventricle to changes in aortic arch pressure in anaesthetized dogs

1. Inotropic changes in the left ventricle in chloralose anaesthetized dogs were determined in response to changes in non-pulsatile pressure perfusing the vascularly isolated aortic arch.2. Inotropic responses were assessed by measuring the maximum rate of change of left ventricular pressure (dP/dt max) in preparations in which heart rate, mean ascending aortic pressure and brachiocephalic (i.e. carotid sinus and cerebral) perfusion pressure were held constant.3. dP/dt max increased (average +43%) when aortic pressure was reduced from a level above that which produced maximum depression of the myocardium to a level below which no further responses could be obtained; responses occurred as aortic arch pressure was changed between 250 and 90 mm Hg.5. In the same preparations changes in the brachiocephalic artery perfusion pressure with aortic arch pressure held constant resulted in similar inotropic responses.6. It is suggested that aortic arch baroreceptors may be of importance in the control of the inotropic state of the heart.     

Reflex responses from the main pulmonary artery and bifurcation in anaesthetised dogs

This study was undertaken to determine the reflex cardiovascular and respiratory responses to discrete stimulation of pulmonary arterial baroreceptors using a preparation in which secondary modulation of responses from other reflexes was prevented. Dogs were anaesthetised with -chloralose, artificially ventilated, the chests widely opened and a cardiopulmonary bypass established. The main pulmonary arterial trunk, bifurcation and extrapulmonary arteries as far as the first lobar arteries on each side were vascularly isolated and perfused through the left pulmonary artery and drained via the right artery through a Starling resistance which controlled pulmonary arterial pressure. Pressures distending systemic baroreceptors and reflexogenic regions in the heart were controlled. Reflex vascular responses were assessed from changes in perfusion pressures to a vascularly isolated hind limb and to the remainder of the subdiaphragmatic systemic circulation, both of which were perfused at constant flows. Respiratory responses were assessed from recordings of efferent phrenic nerve activity. Increases in pulmonary arterial pressure consistently evoked increases in both perfusion pressures and in phrenic nerve activity. Both vascular and respiratory responses were obtained when pulmonary arterial pressure was increased to above about 30 mmHg. Responses increased at higher levels of pulmonary arterial pressures. In 13 dogs increases in pulmonary arterial pressure to 45 mmHg increased systemic perfusion pressure by 24 +/- 7 mmHg (mean +/- S.E.M.) from 162 +/- 11 mmHg. Setting carotid sinus pressure at different levels did not influence the vascular response to changes in pulmonary arterial pressure. The presence of a negative intrathoracic pressure of -20 mmHg resulted in larger vascular responses being obtained at lower levels of pulmonary arterial pressure. This indicates that the reflex may be more effective in the intact closed-chest animal. These results demonstrate that stimulation of pulmonary arterial baroreceptors evokes a pressor reflex and augments respiratory drive. This reflex is likely to be elicited in circumstances where pulmonary arterial pressure increases and the negative excursions of intrathoracic pressure become greater. They are likely, therefore, to be involved in the cardio-respiratory response to exercise as well as in pathological states such as pulmonary hypertension or restrictive or obstructive lung disease.     

Comparison of aortic and carotid baroreflexes in the dog

1. Experiments with vascularly isolated, blood-perfused aortic arch and carotid sinus preparations in sixteen dogs have provided evidence which suggests that, in the reflex regulation of normal arterial blood pressure, the aortic and carotid baroreflexes are not equivalent.2. Two different techniques were used. In one, a steel cannula was inserted into the ascending aorta and arch and fixed in position by ligatures about the aorta. The blood-filled space (aortic jacket) thus created could be distended with known pressures; the cardiac output passed through the cannula into the descending aorta. In the other, an extracorporeal circulation utilizing an isolated heart-lung preparation was used to separately perfuse the carotid sinuses, aortic arch, and systemic circulation of a test dog.3. Independent open-loop analysis of the aortic and carotid baroreflexes in each dog indicated that they were essentially similar in their over-all modus operandi but that there were quantitative differences between them which would suggest a predominant role for the carotid sinus reflex in the control of normal blood pressure.4. The carotid sinus Blutdruck-charakteristik curve was symmetrical about the range of normal blood pressure for the dog while the aortic arch curve was displaced to the right.5. The carotid sinus system had the greater gain (with reference to limb vascular resistance) and exhibited a greater maximal capacity to alter vascular resistance reflexly.6. When the carotid and aortic systems were activated simultaneously by distension, the reflex depressor responses were summed, essentially by a process of simple addition. A carotid-induced pressor response obscured a simultaneous aortic-induced depressor response of equal magnitude.7. In five dogs studied, the functional reflexogenic area of the aortic arch did not extend distally beyond the origin of the left subclavian artery.     

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.     

The responses of aortic arch and right subclavian baroreceptors to changes of non-pulsatile pressure and their modification by hypothermia

1. A method is described for isolation of the aortic arch and right subclavian-carotid angle in situ in the rabbit and perfusion with Krebs-Henseleit solution or blood under controlled conditions of pressure and temperature.2. The characteristics of the baroreceptors of the aortic arch and right subclavian-carotid angle were studied by recording from single or few-fibre preparations of the left and right aortic nerves respectively. Curbes were plotted to show the relationship between the frequency of baroreceptor impulse activity and intra-aortic pressure during non-pulsatile perfusion under steady-state conditions.3. The aortic arch and right subclavian-carotid angle baroreceptors were found to have similar characteristics. Three types of response of the baroreceptors at the threshold pressure to a steady intra-aortic pressure are described.4. Increasing the intra-aortic pressure increased the frequency of impulses in fibres previously active and caused recruitment of other fibres in multi-fibre preparations. The relationship was linear at low pressures and a point of inflexion occurred at higher pressures in the majority of fibres.5. Lowering the temperature of the perfusate reduced the impulse frequency at any given pressure.6. The curves obtained during stepwise increases and decreases in intra-aortic arch pressure were dissimilar, particularly at the lower end of the pressure range. This phenomenon is probably due to properties of the arterial wall.7. When the aortic arch preparation was excised, changes occurred in the shape of the impulse frequency-pressure curves from baroreceptors in both areas. The point of inflexion was elevated and a higher percentage of fibres failed to reach a point of inflexion in the pressure range studied.     

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.     

The effect of baroreceptors on the latency of evoked responses in sympathetic nerves during the cardiac cycle

1. A rapid increase in pressure in a vascularly isolated perfused carotid sinus has been shown to inhibit a reflex response in efferent sympathetic nerves of the dog evoked by electrical stimulation of the radial nerve.2. In intact preparations with the carotid baroreceptors innervated, the mean latency and the variance of the latency of reflex sympathetic nerve responses was reduced when the stimuli evoking the responses were applied at one point of both cardiac and respiratory cycles. When the baroreceptors were denervated there were no significant differences in the responses to random and synchronized stimuli.3. In intact preparations the latency of evoked responses in sympathetic nerves was found to vary progressively during a cardiac cycle; the maximum increase in latency was observed with the responses that occurred at that phase of the cardiac cycle when the baroreceptors exert maximal inhibition on spontaneous sympathetic activity. After denervation of the carotid sinuses a much smaller change during the cardiac cycle was still present, possibly due to effects produced by baroreceptors of the aortic arch and elsewhere.4. It was concluded that changes in baroreceptor activity, due to beat to beat fluctuations of the systemic arterial pressure are a major factor causing variations in the latency of responses in sympathetic nerves evoked by stimuli applied to a cutaneous nerve.     

The influence of aortic baroreceptors on venous tone in the perfused hind limb of the dog.

1. The aortic arch and both carotid sinuses were vascularly isolated and perfused. A hind limb was vascularly isolated and blood was pumped at constant flows into the femoral artery and the central end of a superficial metatarsal vein. 2. Large increases in aortic arch pressure resulted in decreases in arterial blood pressure, heart rate and femoral arterial perfusion pressure. The average response of the vein was a decrease of 11% in the pressure gradient between the perfused vein and the femoral vein. Similar responses were obtained when carotid sinus pressure was increased. 3. Crushing or cooling the lumbar sympathetic trunk caused responsed similar to those induced by increasing baroreceptor perfusion pressure. Stimulation at 1 HZ resulted in venous responses four times as great as the average reflex response, whereas frequencies of 2-5 Hz were required to produce changes in arterial resistance as great as those induced reflexly. 4. These experiments indicate, that although the large superficial veins of the dog's hind limb participate in the baroreceptor reflexes, the activities in the nerves supplying arterioles and veins must have been different.     

Influence of pulsatile perfusion upon renin release from the isolated perfused rat kidney

It is well established that renin release from the juxtaglomerular epithelioid cells in the media of the afferent arteriole strongly depends on the mean renal perfusion pressure, whereas a possible influence of the pulsation of blood pressure on renin release has only occasionally been investigated, and the results are contradictory. Such an influence on renin release cannot be excluded because pulsation is known to modulate arterial baroreceptors and vascular tone in some resistance vessels. In the isolated perfused rat kidney, we found a pulsation amplitude-dependent inhibition of renin release that could be blocked either by vasodilatation or by calcium channel blockade. The inhibition occurred at perfusion pressures between 85 and 125 mm Hg. The underlying pulsation pressure-sensitive mechanism has to be ascribed integrating properties, because a constantflow pressure rise to the “systolic” value of pulsatile perfusion resulted in virtually the same inhibition of renin release. Moreover, a reduced urine flow during pulsatile perfusion provides evidence for preglomerular constriction under these conditions. It is concluded that, besides pathological changes of renal perfusion pressure, variations of the pulse amplitudes, e.g. resulting from renal artery stenosis or atherosclerosis, may also influence renin release and contribute to renovascular hypertension.     

The vasomotor component of the carotid sinus baroreceptor reflex in the cat during stimulation of the hypothalamic defence area

1. The effect of moderate intensities of stimulation of the hypothalamic defence area on the baroreceptor reflex has been investigated in the cat by comparing the responses of arterial blood pressure and perfusion pressure of the isolated hind-limb muscle bed perfused at constant volume inflow, when the isolated carotid sinus was subjected to a series of non-pulsatile pressures with and without simultaneous hypothalamic stimulation.2. In the absence of hypothalamic stimulation the characteristic sigmoid curves relating sinus pressure to blood pressure or muscle perfusion pressure were obtained.3. With simultaneous stimulation of the hypothalamus a similar sigmoid relationship was found. There was no evidence of any reduction in the over-all power or maximum sensitivity of the baroreceptor reflex.4. However, in those cats which had been atropinized to abolish the cholinergically mediated muscle vasodilatation, the curves obtained during hypothalamic stimulation were displaced in such a manner as to suggest that, while baroreceptor modulation of vasoconstrictor tone continued during defence area stimulation, the blood pressure regulating mechanism had been ;reset' so that, within the physiological range of sinus pressures, any given level of sinus pressure was associated with a greater vasoconstrictor tone.5. In non-atropinized cats there was little displacement of the curves relating sinus pressure to blood pressure, while the curves relating sinus pressure to muscle perfusion pressure were displaced in the opposite direction so that over-all muscle vascular resistance was less than normal at each level of sinus pressure.     

Lack of interaction between adenosine-induced vasodilatation and carotid baroreflex-induced changes in sympathetic activity in dog hindlimb artery

In anaesthetized dogs, a hindlimb was vascularly isolated and perfused at a constant flow rate of 7.7 +/- 1.9 ml min-1 100 g-1 (mean +/- S.E.M.; n = 5) through the femoral artery. The carotid sinuses were isolated and perfused at high (greater than 145 mmHg) or low (less than 75 mmHg) pressure to enable reflex sympathetic tone on the hindlimb vessels to be controlled. Both vagi were sectioned in the neck and mean aortic blood pressure was held constant by connection of the aorta to a reservoir. The responses to infusion of three doses of adenosine at high and low carotid sinus pressures were not significantly different: infusion of 0.60 +/- 0.16 microM-adenosine reduced femoral arterial perfusion pressure (FAPP) by 11.6 +/- 3.2% (n = 6) at high carotid sinus pressure and by 12.6 +/- 5.1% (n = 4) at low carotid sinus pressure, while 4.71 +/- 0.49 microM-adenosine reduced FAPP by 20.8 +/- 4.8% (n = 6) at high carotid sinus pressure and by 20.7 +/- 4.8% (n = 6) at low carotid sinus pressure; 50.1 +/- 7.3 microM-adenosine reduced FAPP by 36.7 +/- 5.5% (n = 6) at high carotid sinus pressure and by 27.7 +/- 7.8% (n = 5) at low carotid sinus pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

A comparison of the stimulus-response curves of aortic and carotid sinus baroreceptors in decerebrated cats

Recordings of total nerve activity suggested differences in the sensitivities and working ranges between aortic and carotid sinus baroreceptors. This result however, conflicts with single fibre studies from isolated receptor zones. Thus it appeared of some interest to compare the function curves of aortic and carotid sinus baroreceptors in the intact animal.This was achieved by comparing the response characteristics of two groups of aortic and carotid sinus baroreceptors in decerebrated cats. One smaller group consisted of 11 receptor pairs, each member of the pair being studied simultaneneously in the same cat, and a larger group consisting of 98 aortic and 49 carotid sinus baroreceptors studied independently of each other.The response of each receptor to wide pressure variations was recorded by inflating and deflating an intraaortic catheter tip balloon. Function curves were derived by plotting receptor discharge in terms of spikes per second against mean aortic pressure. No significant differences were found either in the slope of the function curves or their mean pressures at minimum activity, the latter appearing to be set by the working blood pressure level.Thus it was concluded that aortic and carotid sinus baroreceptors differ neither in their sensitivities nor in their working ranges when in their physiological environment.The support of the Deutsche Forschungsgemeinschaft through the Sonderforschungsbereich 30, Kardiologie Düsseldorf is gratefully acknowledged     

Responses of abdominal vascular capacitance in the anaesthetized dog to changes in carotid sinus pressure.

1. The abdominal circulation of anaesthetized dogs was vascularly isolated without opening the abdomen, by cutting or tying all structures immediately above the diaphragm and tying the proximal ends of the hind limbs. The region was perfused at constant flow through the aorta and drained at constant pressure from the inferior vena cava. 2. Vascular resistance responses were expressed as the changes in perfusion pressure and capacitance responses were determined by integrating changes in vena caval outflow. 3. Decreasing the pressure in the isolated carotid sinuses over the whole baroreceptor sensitivity range increased mean perfusion pressure from 91 to 149 mmHg (a 67% increase in resistance) and decreased mean capacitance by 111 ml. (5 ml. kg-1). 4. The range of carotid sinus pressures over which capacitance responses occurred was at a significantly higher level than the corresponding range for resistance responses. 5. Comparison of the reflex responses with the responses to direct stimulation of efferent sympathetic nerves shows that quantitatively similar responses of resistance and capacitance to those induced by a large step decrease in carotid pressure could be produced by stimulating maximally the efferent sympathetic nerves at 5 Hz. These results also suggest that at all levels of carotid sinus pressure there is no difference in the impulse traffic to resistance and capacitance vessels.     

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.     

The effects of changes in the carotid sinus baroreceptor activity on splanchnic blood flow in anesthetized man

In 9 patients being subjected to abdominal surgery, electromagnetic blood flow measurements were obtained from the hepatic, mesenteric and iliac beds while the carotid sinus baroreceptors were stimulated by carotid sinus massage. Carotid sinus stimulation produced an average maximum decrease in mean arterial pressure of 21%. Hepatic and mesenteric blood flows decreased by 15% and calculated vascular resistances were not significantly changed in these vascular beds. Iliac blood flow, on the other hand, showed a slight increase and iliac vascular resistance was decreased by 29%. It is concluded that the splanchnic vascular bed is of less importance in the carotid sinus baroreflex control of systemic arterial pressure in anesthetized man.     

Influence of carotid baroreceptors on different components of the vascular system

1. Reflex changes in wall tension of the lateral saphenous vein of one hind limb, the splenic veins and capsule, and the resistance vessels of the other hind limb caused by changes in baroreceptor activity were measured in vagotomized dogs under thiopentone-chloralose anaesthesia.2. Three different methods were used to alter pressure in one or both carotid sinuses. (1) Both carotid sinuses were vascularly isolated and filled with fully oxygenated Krebs-Ringer bicarbonate solution (pH 7.4) from a reservoir in which the pressure could be altered at will. (2) One sinus was denervated, and the contralateral sinus was perfused with arterial blood at different flow rates. (3) One sinus was denervated, and the innervated sinus was perfused with arterial blood at constant flow, the pressure being altered by changing the outflow resistance.3. The left saphenous vein was perfused at constant flow with autologous blood; changes in perfusion pressure were used as a measure of changes in veno-motor activity. The right common iliac artery was perfused at constant flow to measure changes in resistance vessel activity. Blood flow through the spleen was temporarily arrested, trapping a fixed volume of blood in the organ. Under these conditions, changes in splenic vein pressure were a measure of changes in smooth-muscle tension in the splenic capsule and veins.4. In order to assess the responses to baroreceptor stimulation in terms of alterations in sympathetic nerve traffic to different components of the peripheral vascular system, ;frequency-response curves' were constructed for spleen, saphenous vein, and limb resistance vessels by electrical stimulation of the splenic nerves and lumbar sympathetic chains.5. The saphenous vein showed no consistent response to changes in baroreceptor activity. Reduction in carotid sinus pressure from 180 to 100 mm Hg caused an increase in venous pressure in the isovolumetric spleen and in the iliac artery perfusion pressure. These results were confirmed by electrical stimulation of the carotid sinus nerve. Whereas the peak responses of the limb resistance vessels corresponded to an increase in lumbar sympathetic nerve traffic of 6-10 c/s, the maximal splenic responses were equivalent to an increase in splenic nerve traffic of 1-4 c/s. These results are consistent with selective autonomic nervous control of different components of the peripheral vascular system.