Evidence for central reorganization of ventilatory chemoreflex pathways in the cat during regeneration of visceral afferents in the carotid sinus nerve

There are two sets of peripheral arterial chemoreceptors in the cat, the carotid bodies innervated by the carotid sinus nerve and the aortic bodies with afferents in the aortic depressor nerves. Reflex stimulation of ventilation in response to hypoxia is abolished acutely after interrupting the sensory pathway from the carotid body chemoreceptors in the cat even though the reflex pathway from the aortic body chemoreceptors is intact. However, in chronically maintained preparations, there is a restoration of the hypoxic response which is mediated by the aortic chemoreflex pathway. It was proposed that restoration was due to a ‘central reorganization’ of chemoreflex pathways which followed interruption of the sensory pathway from the carotid bodies and that the reorganization enhanced the efficacy of the aortic ventilation chemoreflex. This proposal was tested in the present experiments by measuring reflex ventilatory and cardiovascular responses to electrical stimulation of the sensory nerves containing aortic and carotid chemoreceptor afferents following bilateral interruption of carotid sinus nerves and carotid body resection. Responses measured acutely (1–6 h) after interruption were compared with those measured 60–80 and 110–140 days later. At 60–80 days, a chemoreflex response (increase in tidal volume of ventilation) to stimulation of the interrupted carotid sinus sensory pathway was markedly attenuated while the response to stimulation of the uninterrupted pathway in aortic depressor nerves was enhanced. At 110–140 days, the tidal volume response to carotid sinus nerve stimulation was greatly enhanced while the aortic depressor nerve response declined from the elevated level. There were significant but less pronounced changes in the response of other ventilatory and cardiovascular variables to aortic depressor nerve and carotid sinus nerve stimulation.The results support the idea that there is a ‘central reorganization’ of chemoreflex pathways which is reflected functionally by changes in the efficacy of reflexes evoked from aortic depressor nerve and carotid sinus nerve. The changes are analagous to those occurring in somatic reflexes during regeneration of sensory nerves. It is suggested that the changes in efficacy of carotid sinus nerve reflexes are due to a degenerative loss of synapses of the central projections of interrupted carotid sinus nerve sensory axons (degenerative atrophy) and subsequent regenerative like changes (regenerative proliferation) in the central projections. The changes in the efficacy of aortic depressor nerve reflexes may be attributed to formation of new synapses by converging central projections of this uninterrupted pathway (reactive synaptogenesis) and subsequent regression of the newly formed synapses.     

Physiological and ultrastructural observations on regenerated carotid sinus nerves after removal of the carotid bodies in cats

Carotid bodies were excised bilaterally in cats and the cut carotid sinus nerves allowed to regenerate freely into the region of the carotid bifurcation for 31 to 315 days. Electrophysiological recordings from regenerated nerves showed spontaneous activity and mechanoreceptive units in some nerves. None of the nerves were excited by physiological or chemical stimuli known to excite chemoreceptors, but electrical stimulation of the regenerated axons evoked reflex ventilatory responses. Serial section light-microscopic analysis of the regenerated nerves revealed bundles of axons branching from the carotid sinus nerve near the site of transection and coursing into the area of the carotid bifurcation. Electron-microscopic examination of the most distal region of the regenerated nerve which could be identified showed axonal bundles comprised of myelinated and unmyelinated fibers characteristic of the mature sinus nerve; axonal sprouts were rarely encountered. Carotid body type 1 or type II cells were never observed. Infrequently, neuronal specializations containing mitochondria and synaptic vesicles were seen in connective tissue in the distal regions of the regenerated nerve. The vascularity of the regenerated nerve was at least comparable to that of the normal carotid sinus nerve.The results indicate that chemoreceptivity is not a property of carotid sinus nerve sensory axons when they are allowed to regenerate freely into the area of the carotid bifurcation after removing the carotid body. Consequently, these observations do not provide support for theories which consider chemoreception to be an intrinsic property of carotid sinus neurons. It is concluded that some extrinsic factor normally provided by the carotid body is essential to the transduction process which initiates depolarization of the sensory axons terminating within this organ.     

Restoration of reflex ventilatory response to hypoxia after removal of carotid bodies in the cat

In mammals there are two sets of peripheral arterial chemoreceptors, the carotid bodies innervated by the sinus branch of the glossopharyngeal nerve and the aortic bodies innervated by the vagus nerves. The afferent impulse discharge from both receptors increases during hypoxia and there is a reflexly mediated increase in ventilation (hypoxic hyperventilation). In the present study we tested this response by exposing anesthetized cats to decreased inspired O₂ concentration before and up to 315 days after bilateral resection of the carotid bodies. Acutely after removing the carotid bodies, hypoxic hyperventilation was abolished. This observation supports the view that the reflex pathway from the aortic body receptors normally contributes minimally to hypoxic hyperventilation. Subsequently, there was a restoration of hypoxic hyperventilation. Restoration was significant 30–43 days after removing the carotid bodies, it reached 70% of the preoperative value at 93–111 days and was essentially complete in terminal experiments 260–315 days after carotid body resection. In terminal experiments, hypoxic hyperventilation was not affected by recutting the regenerated carotid sinus nerves but was abolished completely by bilateral transection of the cervical vagosympathetic trunks. The restored ventilatory response was due predominantly to an increase in rate of breathing while an increase in tidal volume was predominant before carotid body resection. Resting ventilation breathing room air was not consistently decreased after carotid body resection while expired CO₂ was elevated from day 20 to day 111 and at the preoperative level in terminal experiments.It is concluded that restoration of hypoxic hyperventilation in the cat after carotid body resection is mediated by the reflex pathway from aortic body chemoreceptors. The possible contribution of chemo-receptive regenerated carotid sinus nerve axons was excluded. It is suggested that restoration may be a consequence of the central reorganization of chemoreceptor afferent pathways consequent to interruption of the carotid body reflex pathway and that as a result the ‘gain’ of the aortic body ventilatory chemoreflex is enhanced.     

The relative roles of the aortic and carotid sinus nerves in the rabbit in the control of respiration and circulation during arterial hypoxia and hypercapnia

1. The respiratory and circulatory effects of graded arterial hypoxia, alone or with superadded hypercapnia, were studied in four groups of unanaesthetized rabbits including normal animals and those with selective section of the aortic nerves, selective section of the carotid sinus nerves and section of both sets of nerves.

2. When measured 2-4 days after selective section of the carotid sinus nerves the resting respiratory minute volume and arterial P_O2 were lower and the P_CO2 higher than normal. These effects were not observed after selective section of the aortic nerves. Selective aortic nerve section, and selective carotid sinus nerve section each produced a similar increase in the resting arterial pressure and heart rate, but were without effect on the resting cardiac output.

3. During arterial hypoxia reflex respiratory and circulatory effects ascribable to arterial chemoreceptor stimulation (hyperventilation, bradycardia, vasoconstriction) were mediated for the most part through the carotid sinus nerve. In animals with only the aortic nerves intact the circulatory response was determined largely by the opposing effects of aortic baroreceptor reflexes and the local peripheral dilator action of hypoxia.

4. The circulatory effects of hyperventilation induced by hypercapnia during arterial hypoxia, in animals with both aortic and carotid sinus nerves cut were small.

5. The results suggest that relatively few chemoreceptor fibres originate from the aortic region in the rabbit, though the carotid sinus and aortic nerves both contain baroreceptor fibres.

     

Renal and cardiovascular afferent inputs to hypothalamic paraventriculo-spinal neurons

Experiments were done in chloralose-anesthetized cats to identify single units in the paraventricular nucleus of the hypothalamus (PVH) that responded to stimulation of afferent renal nerves (ARN) and the buffer nerves (carotid sinus (CSN) and aortic depressor (ADN) nerves), and whose axons projected directly to thoracic spinal sympathetic areas. Of 426 single units tested in the PVH region, 20 were antidromically activated by stimulation of the spinal cord. Sixteen of these antidromic units (80%) responded orthodromically to stimulation of ARN and/or the buffer nerves; 6 units (30%) were excited by ARN stimulation only, 2 units (10%) were excited by both ARN and buffer nerve stimulation, and 6 units were excited and 2 inhibited by buffer nerve stimulation only. These data demonstrate that sensory information originating in renal and cardiovascular receptors alters the firing rate of PVH-spinal projecting neurons and suggest that this long renal-PVH reflex loop may contribute to the elevation of arterial pressure (AP) during conditions when ARN are activated.     

Inferior cardiac nerve activity in the cat during occlusion of the mesenteric artery.

A number of studies in this and other laboratories using hemodynamic and pharmacologic evidence have suggested that occlusion of the mesenteric artery evokes a pressor reflex initiated by mesenteric baroreceptors. To provide additional evidence in support of this hypothesis, neurophysiological recordings were made of inferior cardiac nerve activity during mesenteric artery occlusion (MAO). The results indicate that MAO enhances inferior cardiac nerve activity in the cat, providing that the carotid sinus nerves have been cut. Cutting of the mesenteric nerves further facilitates cardiac nerve activity and abolishes the response to mesenteric artery occlusion. The evidence suggests that MAO evokes a reflex sympathetic discharge which is subject to override by the carotid sinus depressor reflex. The afferent limb of the reflex is characterized by a tonic depressor outflow from the mesenteric pressure receptors.     

Carotid sinus nerve terminals which are tyrosine hydroxylase immunoreactive are found in the commissural nucleus of the tractus solitarius

Summary Tyrosine hydroxylase immunoreactive sensory neurons in the petrosal ganglion selectively innervate the carotid body via the carotid sinus nerve. Central projections of the carotid sinus nerve were traced with horseradish peroxidase. The commissural nucleus of the tractus solitarius was examined by dual labelling light and electron microscopy. Dense bilateral labelling with horseradish peroxidase was found in the tractus solitarius and commissural nucleus of the tractus solitarius. Horseradish peroxidase was found in unmyelinated axons, myelinated axons, and nerve terminals. About 88% of horseradish peroxidaselabelled carotid sinus nerve axons were unmyelinated. Tyrosine hydroxylase immunoreactivity was identified in unmyelinated axons, myelinated axons, dendrites, perikarya, and nerve terminals. Most tyrosine hydroxylase immunoreactive axons (93%) in the commissural nucleus of the tractus solitarius were unmyelinated. Tyrosine hydroxylase immunoreactivity was simultaneously identified in carotid sinus nerve unmyelinated axons, myelinated axons, and nerve terminals. These double-labelled terminals comprised 28% of the number of tyrosine hydroxylase immunoreactive terminals in the commissural nucleus of the tractus solitarius, and 55% of transganglionically-labelled terminals. Therefore, there are both central and peripheral sources of tyrosine hydroxylase immunoreactive nerve terminals in the commissural nucleus of the tractus solitarius. These data support the hypothesis that peripheral tyrosine hydroxylase immunoreactive neurons are involved in the origination of the chemoreceptor reflex. Axo-axonic synapses between peripheral carotid sinus nerve afferent terminals and central terminals containing tyrosine hydroxylase immunoreactivity were observed in 22% of the axo-axonic synapses observed. Thus, central tyrosine hydroxylase immunoreactivity neurons are involved in the modulation of the chemo- and/or baroreceptor reflexes. Synaptic contacts were not observed between carotid sinus nerve afferents and tyrosine hydroxylase immunoreactive perikarya of dendrites. Catecholaminergic neurons are thus unlikely to be the second order neurons of either the chemo- or baroreceptor reflex in the commissural nucleus of the tractus solitarius.     

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.     

Hypoxia inhibits baroreflex vagal bradycardia via a central action in anaesthetized rats

It is known that arterial baroreflexes are suppressed in stressful conditions. The present study was designed to determine whether and how hypoxia affects arterial baroreflexes, especially the heart rate component, baroreflex vagal bradycardia. In chloralose-urethane-anaesthetized rats, baroreflex vagal bradycardia was evoked by electrical stimulation of the aortic depressor nerve, and the effect of 15 s inhalation of hypoxic gas (4% O2) was studied. Inhalation of hypoxic gas was found to inhibit baroreflex vagal bradycardia. The inhibition persisted after bilateral transection of the carotid sinus nerve. Cervical vagus nerves were cut bilaterally and their peripheral cut ends were stimulated to provoke vagal bradycardia of peripheral origin so as to determine whether hypoxia could inhibit vagal bradycardia by acting on a peripheral site. In contrast to baroreflex vagal bradycardia, the vagus-induced bradycardia was not affected by hypoxic gas inhalation. It is concluded that baroreflex vagal bradycardia is inhibited by hypoxia and the inhibition is largely mediated by its direct central action.     

Local and reflex factors affecting the distribution of the peripheral blood flow during arterial hypoxia in the rabbit

1. The effects of severe arterial hypoxia on the blood flow in the portal vein, and in kidney, muscle and skin beds have been determined in normal unanaesthetized rabbits, in animals without functioning autonomic effectors, and in rabbits with section of the carotid sinus and aortic nerves.

2. The resting blood flows in the above regions were not significantly different in the three groups.

3. The susceptibilities of the various beds to the local dilator effects of arterial hypoxia (assessed from the responses of animals without functioning autonomic effectors) were markedly different; vasodilatation was by far the greatest in the portal bed, followed in order by the renal, skin and muscle beds.

4. Section of the carotid sinus and aortic nerves completely abolished reflex activity, and the pattern of peripheral blood flow changes was similar to that of animals without functioning autonomic effectors. The findings suggest that the arterial chemoreceptors are the primary afferent source of reflex control of the peripheral circulation in arterial hypoxia.

5. In normal animals with intact reflexes there was sustained vasoconstriction throughout the treatment period in the portal and renal bed. The net vasomotor effects in muscle and limb skin were small owing to the operation of a number of factors, which opposed the effects of reflexly increased sympathetic nerve activity.

     

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.     

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.     

Circulatory control in hypoxia by the sympathetic nerves and adrenal medulla

1. The effects of severe arterial and primary tissue (carbon monoxide) hypoxia on cardiac output, arterial and right atrial pressures, heart rate and ventilation, have been studied in unanaesthetized normal rabbits, and in animals subjected to adrenalectomy, ;sympathectomy' (guanethidine), adrenalectomy + ;sympathectomy', and section of the carotid sinus and aortic nerves.2. In both arterial and primary tissue hypoxia the sympathetic nerves play a more important part in the normal circulatory response than the adrenal medullary hormones.3. Provided one adrenergic effector pathway remains intact, animals with intact chemoreceptors and baroreceptors tolerate both types of hypoxia well. Circulatory control during both types of hypoxia by means of sympathetic nerves alone produces relatively more peripheral vasoconstriction than is observed during reflex control through increased adrenal catecholamine secretion.4. The occurrence of tonic sympathetic activity in animals with section of carotid sinus and aortic nerves permits maintenance of a high cardiac output during hypoxia but the arterial pressure is low and there is probably less selective distribution of blood flow to the periphery than in animals with normal reflex control.5. Absence of any adrenergic activity in adrenalectomized and ;sympathectomized' animals results in a gradual fall in cardiac output during prolonged hypoxia, after an initial small rise.6. The results in guanethidine-treated animals suggest that the sympathetic discharge to the arterial chemoreceptors is a factor sustaining chemoreceptor discharge during prolonged arterial hypoxia.     

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 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.     

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     

Rabbit cardiovascular responses to aortic nerve stimulation at fixed carotid pressure.

In pentobarbital-anesthetized rabbits with aortic nerves cut, reflex heart rate and mean arterial pressure (MAP) changes were quantified in response to maximal central stimulation of the left aortic nerve (LANS) before and during steady-state changes in isolated carotid intrasinus pressure (ISP). To distinguish possible vagally mediated cardiopulmonary influences, responses were measured before and after vagotomy. Changes in MAP observed by altering ISP within +/- 15 mmHg of the equilibrium pressure (EP) were linear and inversely correlated to changes in ISP, with a slope of approximately 3 both before and after vagotomy (r greater than or equal to 0.929, P less than 0.05). The peak fall in MAP during LANS was dependent upon ISP. The change in the MAP responses to LANS for each mmHg change in ISP ranged from 1.7 with vagi intact to 1.3 after vagotomy. Heart rate was unaltered by isolation of the carotid sinus and was independent of the small changes in ISP between +/- 15 mmHg of EP. These results indicate that blood pressure changes elicited by the aortic baroreflex are extremely sensitive to the degree of carotid sinus compensation. Thus, to assess the sensitivity of any arterial reflex area, the existing level of compensation by other barosensitive areas must be known.     

The effects of electrical stimulation of the distal end of the cut sinus and aortic nerves on peripheral arterial chemoreceptor activity in the cat

1. In anaesthetized cats, stimulation of efferent components of the carotid sinus or aortic nerves depressed chemoreceptor discharge from the relevant chemoreceptor afferents. The local application of 2% procaine hydrochloride to the sinus nerve trunk, peripheral to the site of the stimulating electrodes and proximal to that of the afferent nerve twig, abolished the depression of afferent chemoreceptor discharge caused by electrical stimulation; on washing the procaine away electrical stimulation once more induced depression of chemoreceptor discharge.2. The depressant effect of efferent stimulation on carotid chemoreceptor activity was still seen during complete carotid glomeral ischaemia. Atropine given by close intra-arterial injection to the carotid body did not affect the depressant influence of efferent sinus nerve stimulation on carotid body chemoreceptor discharge.3. Stimulation of the sinus nerve efferents usually increased carotid body blood flow. Close arterial injection of atropine abolished this effect.4. The responses of glomeral blood flow and carotid chemoreceptor activity to efferent stimulation of the cut sinus nerve were not temporally related. It seems improbable that the depressant effect of such stimulation on chemoreceptor discharge was due to alterations of glomeral blood flow.5. Stimulation of the peripheral end of the cervical vagus in atropinized cats reduced chemoreceptor activity recorded in the ipsilateral aortic nerve.     

The contribution of the arterial chemoreceptors to the stimulation of respiration by adrenaline and noradrenaline in the cat

1. Intravenous infusions of adrenaline and noradrenaline in doses averaging 0.8 mug/kg.min increased the respiratory minute volume of anaesthetized cats breathing room air. The mean increase in respiratory minute volume was 14% during adrenaline infusion and 8% during noradrenaline infusion.2. In a small group of decerebrate cats infusions of adrenaline and noradrenaline increased ventilation by 19 and 27% respectively.3. Intravenous catecholamine infusions also increased the respiratory responses of anaesthetized animals to the inhalation of 5% or 10% O(2) in N(2) and to the inhalation of 5% CO(2) in air.4. Adrenaline and noradrenaline infusions had no significant effect on the ventilation of animals breathing 100% O(2), nor did they significantly alter the respiratory response to the inhalation of 5% CO(2) in O(2).5. After section of the carotid sinus and aortic nerves, a blood-pressure compensator being used to minimize changes in arterial pressure, catecholamines had no effect on the respiration of cats breathing air.6. An increase in carotid body chemoreceptor discharge accompanied the increase in ventilation during catecholamine infusion.7. Intravenous catecholamine infusions still produced an increase in ventilation and carotid body chemoreceptor discharge after both aortic nerves and both cervical sympathetic nerves had been cut.8. Intra-arterial infusions into one carotid artery of 0.2 mug/kg.min of adrenaline or 0.1 mug/kg.min of noradrenaline led to mean increases in respiratory minute volume of 9.9 and 11.5% respectively. No increase occurred after section of the corresponding carotid sinus nerve. Such infusions also evoked an increase in carotid body chemoreceptor discharge.9. It is concluded that the hyperpnoea produced by adrenaline and noradrenaline infusions in the cat is predominantly reflex in origin and is mediated by the arterial chemoreceptors.10. The increase in ventilation produced by adrenaline appears to have a component additional to its effect upon the chemoreceptors though the nature of this action has not been identified.