Comparison of the reflex vasomotor responses to separate and combined stimulation of the carotid sinus and aortic arch baroreceptors by pulsatile and non-pulsatile pressures in 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. When the vasosensory areas were perfused at non-pulsatile pressures within the normal physiological range of mean pressures, the reflex reduction in systemic vascular resistance produced by a given rise in mean carotid sinus pressure was significantly greater than that resulting from the same rise of aortic arch pressure.3. On the other hand, when the vasosensory areas were perfused at normal pulsatile pressures and within the normal physiological range of mean pressures, there was no difference in the size of the reflex vascular responses elicited by the same rise in mean pressure in the carotid sinuses and in the aortic arch.4. Whereas the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in pulse pressure, those evoked by the aortic arch baroreceptors through changes of mean pressure are only weakly affected by modifications in pulse pressure. Evidence for this was obtained from single stepwise changes of mean pressure in each vasosensory area during pulsatile and non-pulsatile perfusion, and from curves relating the mean pressure in the carotid sinuses or aortic arch and systemic arterial perfusion pressure.5. The vasomotor response elicited by combined stimulation of the carotid sinus and aortic arch baroreceptors was greater than either response resulting from their separate stimulation.6. When the mean perfusion pressures in the two vasosensory areas are changed together, the curve relating mean pressure to systemic arterial pressure during pulsatile perfusion of the areas is considerably flatter than that for non-pulsatile perfusion.7. Increasing the pulse pressure in the carotid sinuses or aortic arch caused a decrease in systemic vascular resistance, the response elicited from the carotid sinuses being the larger.8. Altering the phase angle between the pulse pressure waves in the carotid sinuses and aortic arch had no effect on systemic vascular resistance.9. In both vasosensory areas, increasing the pulse frequency caused a reduction in systemic vascular resistance.     

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.     

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.     

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.     

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.     

The effect of time of electrical stimulation of the carotid sinus on the amount of reduction in arterial pressure

Summary On narcotised dogs, the carotid sinus nerve was stimulated by means on electrical R-wave-triggered pulse trains when depressor nerves were either intact or cut.The stimulation was begun in the range from 0–210 msec after the R-wave. The effectiveness of pulse trains was determined by the level of reduction in mean arterial pressure.In the time range studied, the level of reduction in pressure versus time of stimulation shows two maxima of reduction at 30 and 90 msec and a plateau from 110–150 msec. Stimuli applied later than 150 msec after the R-wave, display a contnuous reduction in effectiveness.The occurrence of the maxima is considered to be due to a coincidence of the pressor afferences from heart, aortic arch and carotid sinus, arriving at the circulatory centres spaced in time with the electrical stimuli.The times at which the maxima of reduction are found to occur could be significant in programming baropacers.     

The cause of the difference between the arterial baroreceptor reflex under natural pulsatile circulation and under nonpulsatile systemic circulation

In a previous study we investigated the relation between afferent and efferent activity of the arterial baroreceptor reflex under nonpulsatile systemic circulation using total left heart bypass. The results indicated that the regulation of the arterial baroreceptor reflex was converted under nonpulsatile systemic circulation, and we inferred that a possible reason for this conversion was the transformation in discharge of the afferent activity of the arterial baroreceptor reflex that took place under nonpulsatile systemic circulation. In the present study we tested this hypothesis by sectioning carotid sinus and aortic depressor nerves and electrically stimulating bilateral aortic depressor nerves under anesthesia in five rabbits (400 spikes for 20s, with 0.02ms pulse width and 8 V amplitude), while recording changes in aortic pressure, mean aortic pressure, and heart rate. Continuous stimulation was taken as discharge of the afferent activity of the arterial baroreceptor reflex under nonpulsatile systemic circulation, and periodic stimulation was taken as discharge under natural pulsatile circulation. Aortic pressure, mean aortic pressure, and heart rate decreased under both continous and periodic stimulation. The decreases in mean aortic pressure and heart rate during continuous stimulation were significantly lower than those during periodic stimulation. Our results suggest that the transformation in discharge of the afferent activity of the arterial baroreceptor reflex under nonpulsatile systemic circulation may have played an important causative role in the conversion of the regulation of the arterial baroreceptor reflex under nonpulsatile systemic circulation.     

Cardiovascular responses in apnoeic asphyxia: role of arterial chemoreceptors and the modification of their effects by a pulmonary vagal inflation reflex

1. In the spontaneously breathing anaesthetized dog, the systemic circulation was perfused at constant blood flow; there was no pulmonary blood flow and the systemic arterial blood P(O2) and P(CO2) were controlled independently by an extracorporeal isolated pump-perfused donor lung preparation. The carotid and aortic bodies were separately perfused at constant pressure with blood of the same composition as perfused the systemic circulation.2. Apnoeic asphyxia, produced by stopping the recipient animal's lung movements and, at the same time, making the blood perfusing the systemic circulation and the arterial chemoreceptors hypoxic and hypercapnic by reducing the ventilation of the isolated perfused donor lungs, caused an increase in systemic vascular resistance.3. While the systemic arterial blood was still hypoxic and hypercapnic, withdrawal of the carotid and aortic body ;drive' resulted in a striking reduction in systemic vascular resistance. Re-establishing the chemoreceptor ;drive' immediately increased the vascular resistance again.4. Apnoeic asphyxia carried out while the carotid and aortic bodies were continuously perfused with oxygenated blood of normal P(CO2) had little or no effect on systemic vascular resistance.5. The systemic vasoconstrictor response produced by apnoeic asphyxia was reduced or abolished by re-establishing the recipient animal's lung movements, and this effect occurred in the absence of changes in the composition of the blood perfusing the systemic circulation and arterial chemoreceptors. This abolition of the vasoconstriction was due to a pulmonary reflex.6. Apnoeic asphyxia slowed the rate of the beating atria due to excitation of the carotid and aortic body chemoreceptors. This response can be over-ridden by an inflation reflex arising from the lungs.7. It is concluded that the cardiovascular responses observed in apnoeic asphyxia are due, at least in part, to primary reflexes from the carotid and aortic body chemoreceptors engendered by arterial hypoxia and hypercapnia. The appearance of these responses is, however, dependent upon there being no excitation of a pulmonary (inflation) vagal reflex.     

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     

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.     

Hypoxaemia and aortic chemoreceptor function in foetal lambs

1. In foetal lambs the effect of raising and lowering arterial P(O2) (by varying the O(2) content of the maternal inspired gas mixture) was studied in order to determine whether the systemic arterial chemoreceptors regulated the circulation.2. From 0.7 of term relative hypoxaemia (e.g. reducing carotid P(O2) from 40 to 20 mm Hg) caused a rise of arterial pressure and femoral vaso-constriction. These changes were unaffected or even increased by bilateral section of the nerves from the carotid sinus and body. They were abolished by section of the vagi or aortic nerves.3. It is concluded that in foetal lambs during the last third of gestation the circulation is under reflex control by the aortic chemoreceptors.     

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.     

The contribution of alterations in cardiac output to changes in arterial pressure reflexly evoked from the carotid sinus in the rabbit.

1. The reflex cardiovascular effects of changes in pressure within the vascularly isolated carotid sinus were examined in seventeen anaesthetized rabbits. The opposite sinus was denervated and both aortic nerves were divided, 2. Comparison of the mean values at sinus pressures of 40 and 200 mmHg showed a large reduction in systemic arterial pressure from 126 to 58 mmHg and a moderate reduction in heart rate, from 287 to 253 beats min-1. Cardiac output, measured by thermal dilution, showed only a small change, a fall from 160 to 148 ml. min-1 kg-1. 3. By contrast with this reduction in cardiac output of just over 7%, total peripheral resistance, derived by dividing mean arterial pressure by cardiac output, was halved, falling from 0-48 to 0-41 mmHg ml.-1 min kg. 4. Thus in the anaesthetized rabbit changes in cardiac output make only a small contribution to the changes in systemic pressure evoked by alterations in carotid sinus pressure. Changes in total peripheral resistance are principally responsible for the effect on systemic pressure. 5. Though the changes in output of the heart were small, there were considerable changes in the work done by the left ventricle which was approximately halved when carotid sinus pressure was raised from 40 to 200 mmHg.     

Reflex discharge patterns of cardiac vagal efferent fibres

1. Unit activity was recorded from single and few fibre preparations in a cardiac branch of the right vagus nerve of the cat.2. Increases in blood pressure mediated solely by the right carotid sinus nerve produced bradycardia when all other nerves to the heart had been cut. Myelinated fibres in the cardiac branch of the right vagus nerve were reflexly activated by the same procedure.3. The fibres were silent when blood pressure was below 140-150 mm Hg. As the pressure began to rise, they discharged phasically with the cardiac cycle. At pressures greater than 180 mm Hg, the discharge was continuous attaining maximum rates of 40/sec.4. Stimulation of carotid body chemoreceptors also reflexly excited these fibres, as did stimulation of baroreceptors in both the left carotid sinus and aortic arch. Afferent fibres in the left vagus discharging in response to changes in blood pressure reflexly excited the cardiac efferent fibres. Increases in phrenic motoneurone discharge coincided with inhibition of these fibres. Electrical stimulation of the glossopharyngeal nerve also produced inhibition.     

Temporal and spatial interactions between the carotid sinus and vagally mediated baroreflexes in dogs

We investigated the temporal and spatial interactions between the carotid sinus and aortic arch baroreflex control of arterial pressure in 25 dogs anesthetized with pentobarbital sodium. The carotid sinus baroreceptor region was vascularly isolated to control the intracarotid sinus pressure. A hemorrhage catheter was inserted into the aortic arch. The systemic arterial pressure change after quick mild hemorrhage (2 ml/kg body weight within 1-2 s) was monitored. The open-loop gain of the vagally mediated baroreflex system was estimated from the mean arterial pressure response to the hemorrhage. Three protocols were employed to analyze the interactions. In the first protocol, we determined the effect of different levels of intracarotid sinus pressure on the open-loop gain of the vagally mediated baroreflex system. There was no significant effect. In the second protocol, the open-loop gain of the carotid sinus baroreflex system was determined after vagotomy. In the third protocol, the vagally mediated baroreflex system was activated by the hemorrhage without (spatial interaction) or with (temporal interaction) a delay after changing the intracarotid sinus pressure. The spatial interaction was facilitatory. A temporal interaction was found between the carotid sinus and vagally mediated baroreflex systems, when the delay was less than 30 s.     

Simulation study of a selective cerebral perfusion system with a single centrifugal pump

We previously successfully developed a simple nonroller extracorporeal circulation system (NRECC). In aortic arch surgery, more than two pumps are generally used for systemic perfusion and selective cerebral perfusion (SCP); we developed a new pressure-dependent perfusion system for SCP based on our NRECC and operated by a single centrifugal pump. The cerebral perfusion line was branched from the main perfusion line, and one 15 French and two 12 French cannulae were used for SCP. The perfusion pressure was regulated with a tube occluder. Afterload was changed from 30 to 80 mm Hg, the pressure of the SCP line was increased from 80 to 200 mm Hg, and flow volume was measured. When the afterload was set at 50 mm Hg, according to the increase of perfusion from 80 to 200 mm Hg, the flow volume of the 15 French cannula increased from 280 to 950 ml/min. Under the same conditions, flow volume of the 12 French cannula increased from 160 to 560 ml/min. Sufficient flow volume of the SCP lines was obtained when the SCP line pressure was over 80 mm Hg. As a result of the increased perfusion pressure, the flow volume showed a direct increase. These findings suggest that aortic arch surgery is possible using this SCP system.     

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)     

Cerebrovascular transmural pressure and autoregulation

The cerebral blood flow (CBF) response to changes in perfusion pressure mediated through decreases in arterial pressure, increases in cerebrospinal fluid (CSF) pressure and increases in jugular venous pressure was studied in anesthetized dogs. A preparation was developed in which each of the three relevant pressures could be controlled and manipulated independently of each other. In this preparation, the superior vena cava and femoral vein were cannulated and drained into a reservoir. Blood was pumped from the reservoir into the right atrium. With this system, mean arterial pressure and jugular venous pressure could be independently controlled. CSF pressure (measured in the lateral ventricle) could be manipulated via a cisternal puncture. Total and regional CBF responses to alterations in perfusion pressure were studied with the radiolabelled microsphere technique. Each hemisphere was sectioned into 13 regions: spinal cord, cerebellum, medulla, pons, midbrain, diencephalon, caudate, hippocampus, parahippocampal gyrus, and occipital, temporal, parietal and frontal lobes. Despite 30 mm Hg reductions in arterial pressure or increases in jugular venous pressure or CSF pressure, little change in CBF was observed provided the perfusion pressure (arterial pressure minus jugular venous pressure or CSF pressure depending on which pressure was of greater magnitude) was greater than the lower limit for cerebral autoregulation (approximately 60 mm Hg). However, when the perfusion pressure was reduced by any of the three different methods to levels less than 60 mm Hg (average of 48 mm Hg), a comparable reduction (25–35%) in both total and regional CBF was obtained. Thus comparable changes in the perfusion pressure gradient established by decreasing arterial pressure, increasing jugular venous pressure and increasing CSF pressure resulted in similar total and regional blood flow responses. Independent alterations of arterial and CSF pressures, and jugular venous pressure produce opposite changes in vascular transmural pressure yet result in similar CBF responses. These results show that cerebral autoregulation is a function of the perfusion pressure gradient and cannot be accounted for predominantly by myogenic mechanisms.     

The role of the carotid body chemoreceptors and carotid sinus baroreceptors in the control of cerebral blood vessels

1. Cerebral blood flow was measured in 17 baboons, anaesthetized with pentobarbitone, paralysed with gallamine and mechanically ventilated and in which the right sinus and both aortic nerves had been cut and the left carotid sinus vascularly isolated. Later in each experiment, the head was artificially perfused with femoral arterial blood via the innominate artery.2. Stimulation of the carotid body chemoreceptors with venous blood invariably caused a rise in regional cerebral blood flow whether the head was naturally or artificially perfused. This response was almost completely abolished if the VIIth cranial nerves were cut intracranially.3. Regional cerebral blood flow varied inversely with carotid sinus pressure.4. After the remaining (left) sinus nerve had been cut, the cerebral vascular response to hypoxia was negligible and the response to hypercapnia was markedly reduced. Blood flow then varied with perfusion pressure.5. These results provide further evidence that cerebral blood vessels are reflexly controlled and that the peripheral arterial receptors are involved. Their action is most conspicuous in the vascular response to hypoxia and together with intrinsic factors in the cerebral vascular bed, they determine the size of the vascular response to changes in CO(2) and pressure.     

The reflex effects of alterations in lung volume on systemic vascular resistance in the dog

1. The reflex effects of alterations in lung volume on systemic vascular resistance have been studied in anaesthetized dogs under conditions in which the systemic circulation was perfused at constant blood flow. The pressures in the isolated perfused carotid sinuses and aortic arch, and the arterial blood P_O2 and P_CO2 were maintained constant.

2. A maintained inflation of the lungs produced by injection of air into the trachea caused a fall in systemic arterial perfusion pressure, indicating vasodilatation. The size of the systemic vasodilator response varied directly with the pressure and volume of gas used to inflate the lungs. A similar effect was observed when the tidal volume of lungs ventilated by an intermittent positive pressure was increased.

3. Collapse of the lungs by creating a pneumothorax in closed-chest spontaneously breathing animals evoked a systemic vasoconstrictor response which was reversed when the lungs were re-expanded.

4. These vasodilator responses were abolished by dividing the pulmonary branches of the thoracic vagosympathetic nerves. Evidence is presented that the afferent fibres run in the cervical vagosympathetic nerves and through the stellate ganglia.

5. The responses were unaffected by atropine, but were abolished by hexamethonium, guanethidine and by bretylium tosylate, indicating that they are mediated via the sympathetic nervous system.

6. Evidence is presented that the lungs are a constant course of afferent impulses inhibiting the `vasomotor centre', and that the lung inflation—systemic vasodilator reflex is a potential mechanism operating in eupnoeic breathing.