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PubMed1988

Evidence that maturation of the peripheral chemoreceptors is not complete in childhood.

We examined the hypothesis that the peripheral chemoreceptors contribute a different degree of tone to respiration during exercise in normal young children as compared to adults. To improve resolution of the peripheral chemoreceptor contribution, the studies were conducted during controlled levels of exercise. Peripheral chemoreceptor function was assessed by the hyperoxic (FIO2 = 0.80) switch technique during steady-state, sub-anaerobic threshold exercise during air (FIO2 = 0.21) and midly hypoxic gas (FIO2 = 0.15) breathing in 9 healthy children (mean +/- 1 SD age (years) = 8.2 +/- 1.4) and 10 healthy adults (28.2 +/- 6.5). Ventilation during exercise was significantly greater under hypoxic conditions in both children and adults. During air breathing exercise the mean ventilatory decrease in response to the hyperoxic switch was similar in the two groups (27.9 +/- 10.7% in children and 23.3 +/- 6.3% in adults). In contrast, during hypoxic gas breathing exercise the children demonstrated a much greater decrease in ventilation following the hyperoxic switch (57.9 +/- 3.6%) compared to adults (38.9 +/- 5.5%) (P less than 0.0001). Thus, the peripheral chemoreceptors have a greater role in the exercise hyperpnea during hypoxic exercise in young children as compared to adults, suggesting attenuation of peripheral chemoreceptor function during maturation.

Adult↗
PubMed1992

Actions of carotid chemoreceptors on subretrofacial bulbospinal neurons in the cat.

Thirty-one barosensitive bulbospinal neurons were recorded from the subretrofacial (SRF) nucleus in eight chloralose-anaesthetised, paralysed cats. Close arterial injections of CO2-saturated saline were used to stimulate carotid body chemoreceptors. Seven neurons were abruptly excited and six neurons abruptly inhibited by chemoreceptor stimuli: these were primary responses, independent of changes in blood pressure or central respiratory drive (monitored from the phrenic nerve). A further eight neurons responded only indirectly to chemoreceptor stimuli, showing enhanced modulation of their activity coupled to the enhanced central respiratory drive. The distinction between primary and secondary responses was shown more clearly when central respiratory drive was inhibited by superior laryngeal nerve stimulation. The remaining ten neurons showed no clear response to chemoreceptor stimuli. SRF bulbospinal neurons thus show the same range of responses to chemoreceptor stimuli as the sympathetic neurons they are believed to drive.

Animals↗
PubMed1993

Role of the central and arterial chemoreceptors in the response of gastric tone and motility to hypoxia, hypercapnia and hypocapnia in rats.

The contribution of autonomic nerve activity to stomach tone and motility during central and arterial chemoreceptor excitation or inhibition was analyzed in urethane anesthetized, artificially ventilated rats. Systemic severe hypoxia at end-tidal O2 concentration (FETO2) 6% and systemic hypercapnia at end-tidal CO2 concentration (FETCO2) 6%, 8% and 10% applied for 1 min produced a significant depression in gastric tone and motility. Hypocapnia at 3% FETCO2 increased gastric tone and motility. Hypoxia co-activated both the sympathetic and the vagal efferent gastric nerve branches. Hypercapnia augmented only sympathetic gastric efferent nerve activity but not vagal efferent nerve activity. Hypocapnia slightly increased vagal nerve activity to the stomach. Bilateral denervation of the arterial chemoreceptors significantly attenuated the inhibitory gastric response to hypoxia. Similar attenuation of hypoxia-induced depression of gastric tone and motility was produced by bilateral gastric sympathectomy but not by vagotomy. In contrast, the inhibitory effect of severe hypercapnia and the facilitatory effect of hypocapnia upon gastric tone and motility were unaffected by arterial chemoreceptor denervation, by severance of gastric sympathetic branches or by gastric vagal denervation. Hyperoxia at 90% FETO2 had no effect on the gastric nerve activities, gastric tone or motility. It is concluded that in the rat hypoxia co-activates sympathetic and vagal efferent nerve activities to the stomach via an arterial chemoreceptor reflex, and that hypercapnia activates sympathetic gastric nerve activity via central chemoreceptors. Hypocapnia activates efferent vagal gastric nerve activity. All chemical stimuli except that of hyperoxia have a significant local effect on the gastric tone and motility.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Absence of respiration modulation of carotid sinus nerve inputs to nucleus tractus solitarius neurons receiving arterial chemoreceptor inputs.

The reflex responses to activation of the arterial chemoreceptors are dependent upon when in the respiratory cycle the chemoreceptor stimulus is given. To determine if the respiratory modulation of the chemoreflex occurs within the nucleus tractus solitarius (NTS), intracellular recordings were obtained in pentobarbital-anesthetized, paralyzed and mechanically ventilated cats, from 22 non-respiratory NTS cells which were depolarized following activation of the ipsilateral carotid body chemoreceptors (by close arterial injection of < 100 microliters CO2 saturated bicarbonate). Activation of the ipsilateral carotid body chemoreceptors evoked depolarizations with amplitudes of 2.9-4.6 mV and durations of 2.1-5.9 s. Three of these cells also received a convergent excitatory input from the carotid sinus baroreceptors. Carotid sinus nerve (CSN) stimulation evoked either an excitatory post-synaptic potential (EPSPs) (n = 14, 8 monosynaptic) or an excitatory/inhibitory sequence (EPSP/IPSPs) (n = 8, 1 monosynaptic). CSN evoked PSPs were separately averaged (25-50 sweeps) during periods of phrenic nerve activity and phrenic nerve silence and during periods when the lungs were inflated and when the lungs were deflated. No parameter of the CSN evoked PSPs (latency, peak amplitude, duration) was altered during periods of phrenic nerve activity or lung inflation (all P values > 0.12, Wilcoxon signed-rank test). The results suggest that there is no respiratory modulation of arterial chemoreceptor inputs by either central respiratory drive or lung stretch receptor afferent inputs at this early stage of the reflex arc.

Animals↗
PubMed2005

Hyperglycemic response to hemorrhage is modulated by baroreceptors unloading but not by peripheral chemoreceptors activation.

The aim of this study was to assess the relative participation of carotid baro- and chemoreceptors on plasma glucose and lactate level in response to hemorrhagic hypotension. We also evaluated the effects of selective activation of carotid chemoreceptors. One week before the experiments, male Wistar rats (250-300 g) were submitted to bilateral total carotid denervation (BCD-group), or to bilateral ligature of the carotid body artery (ChD-group). During the same surgical procedure, a chronic jugular catheter for blood sampling and hemorrhage (1.2 mL/100 g/2 min) and polyethylene cannula was inserted into the left femoral artery for cardiovascular monitoring. One group submitted to fictitious surgery was used as a surgical control (Sham-group). Carotid chemoreceptors were selectively activated by sodium cyanide (NaCN, 40 microg/0.1 mL i.v.) in the Sham and ChD group. The results showed that hyperglycemic response to hemorrhage in the BCD-group was reduced whereas in the ChD-group there was no significant change in this parameter compared to the Sham group (8.6 +/- 0.5 mM, Sham-hemorrhaged, n = 8; 7.2 +/- 0.3 mM, BCD-hemorrhaged, n = 8 and 9.4 +/- 0.6 mM, ChD, n = 8, p < 0.05). Increased plasma lactate levels following hemorrhage were observed in all the three experimental groups throughout the experimental period and there were no differences between the groups. Chemoreceptor stimulation by NaCN also produced hyperglycemia, as well as an increase in blood pressure and bradycardia but did not affect plasma lactate concentration. Ligature of the carotid body artery annulled the cardiovascular responses induced by NaCN, but did not change the hyperglycemic response to hypoxia. In conclusion, our data indicate that carotid chemoreceptors do not play any major role in overall metabolic response to hypoxia or hemorrhagic hypotension. Furthermore, the results suggest that carotid baroreceptors unloading play a predominant role as main source of afferent impulses leading to the hyperglycemic response to hemorrhage. In addition our data shows that the metabolic response and cardiovascular adjustment to hypoxia can be dissociated by ligature of the carotid body artery.

Animals↗
PubMed1987

The contribution of peripheral chemoreceptors to ventilation during heavy exercise.

The purpose of this study was to determine, in man, the contribution of peripheral chemoreceptors to ventilation during constant-load, heavy exercise above anaerobic threshold at sea level, using hyperoxic suppression of peripheral chemoreceptor drive which was obtained by abrupt and surreptitious replacement of inspired air with 100% oxygen for a period of 20-30 sec during the exercise. There was a delay of at least 1 sec from the time of peripheral chemoreceptor blockade to the initial change in ventilation, suggesting the operation of a central neural reverberatory mechanism after the cessation of peripheral chemoreceptor drive. In contrast to Wasserman (1976), whose results indicated a 25% decrease in ventilation within two breaths, in the present study no significant drop was observed until some 4-6 breaths after the air-to-oxygen switch. Furthermore, the drop in ventilation, magnitude of which was of the order of 15%, was transient in 5 out of 8 subjects. In one subject, the ventilation increased following oxygen administration. It is concluded that the peripheral chemoreceptors are not the sole mediators of hyperventilation of heavy exercise above anaerobic threshold in man.

Acidosis↗
PubMed1999

CO2, brainstem chemoreceptors and breathing.

The regulation of breathing relies upon chemical feedback concerning the levels of CO2 and O2. The carotid bodies, which detect O2, provide tonic excitation to brainstem respiratory neurons under normal conditions and dramatic excitation if O2 levels fall. Feedback for CO2 involves the carotid body and receptors in the brainstem, central chemoreceptors. Small increases in CO2 produce large increases in breathing. Decreases in CO2 below normal can, in sleep and anesthesia, decrease breathing, even to apnea. Central chemoreceptors, once thought localized to the surface of the ventral medulla, are likely distributed more widely with sites presently identified in the: (1) ventrolateral medulla; (2) nucleus of the solitary tract; (3) ventral respiratory group; (4) locus ceruleus; (5) caudal medullary raphé; and (6) fastigial nucleus of the cerebellum. Why so many chemoreceptor sites? Hypotheses, some with supporting data, include the following. Geographical specificity; all regions of the brainstem with respiratory neurons contain chemoreceptors. Stimulus intensity; some sites operate in the physiological range of CO2 values, others only with more extreme changes. Stimulus specificity; CO2 or pH may be sensed by multiple mechanisms. Temporal specificity; some sites respond more quickly to changes on blood or brain CO2 or pH. Syncytium; chemosensitive neurons may be connected via low resistance, gap junctions. Arousal state: sites may vary in effectiveness and importance dependent on state of arousal. Overall, as judged by experiments of nature, and in the laboratory, central chemoreceptors are critical for adequate breathing in sleep, but other aspects of the control system can maintain breathing in wakefulness.

Animals↗
PubMed1998

The effect of chemoreceptor stimulation on the centripetal transfer of somatosensory information in the urethane-anaesthetized rat.

In urethane-anaesthetized rats, stimulation of carotid body chemoreceptors desynchronizes the cortical electroencephalogram and increases the sensitivity of thalamic and cortical somatosensory neurones to peripheral sensory nerve stimulation. Peripheral chemoreceptors were stimulated by injecting a bolus (30 ml) or infusing 100 ml of 0.18 M NaCl solution equilibrated with 100% CO2 into an internal carotid artery, the cortical electroencephalogram and ventilation were monitored routinely. This stimulus induced hyperventilation and desynchronization of the cortical electroencephalogram. Anaesthetized rats also showed spontaneous periodic increases in ventilation rate accompanied by changes of the cortical electroencephalogram from high-voltage low frequency to low-voltage high frequency which seemed to be identical with those evoked by stimulating chemoreceptors. The activity of identified somatosensory neurons in the thalamic ventrobasal complex, layer IV of the somatosensory cortex, or the cuneate nucleus was recorded extracellularly during and following chemoreceptor activation. Neurones in the ventrobasal thalamus and somatosensory cortex showed a decrease in latency and an increase in probability of discharge to supramaximal electrical stimulation of the forepaw which was more pronounced following infusion stimulation of the carotid body than following bolus stimulation. In contrast, neurons within the cuneate nucleus showed a slight increase in latency to onset and a decrease in the probability of firing following the same stimulus. The results indicate that stimulation of the carotid body chemoreceptors leads to an enhancement of the response of somatosensory neurons to their normal physiological input.

Anesthetics, Intravenous↗
PubMed2002

Atracurium and vecuronium block nicotine-induced carotid body chemoreceptor responses.

BACKGROUND: Vecuronium depresses carotid body chemosensitivity during hypoxia. We hypothesized that this is caused by inhibition of cholinergic transmission of the carotid body. METHODS: The carotid body with its sinus nerve was removed en bloc from thiopentone-anaesthetized adult male New Zealand rabbits and perfused in vitro with modified Tyrodes buffer solution at constant perfusion pressure, temperature, a buffer pH of 7.4 and normocapnia. Chemoreceptor discharge and spike frequencies (fx) were recorded from the whole sinus nerve after administration of 500 microg nicotine, given as duplicated controls and thereafter following 30 min perfusion of equipotent concentrations of atracurium (28.1 microM) or vecuronium(10 microM), after 30 min of neostigmine perfusion (9.2 microM) and finally after 30 min wash-out with buffer solution only. A short-lasting hypoxic test was performed before and at the end of the experimental period to confirm the responsiveness and validity of the preparation. RESULTS: Atracurium (n = 7) and vecuronium (n = 6) reduced chemoreceptor responses to nicotine by 70 +/- 30% and 66 +/- 19% (SEM) (P<0.05). Chemoreceptor discharges showed full recovery after neostigmine in the atracurium group and partial recovery in the vecuronium group (P<0.05). Finally, after wash-out the chemoreceptor responses to nicotine had fully recovered in both groups. CONCLUSION: Atracurium and vecuronium in equipotent concentrations block nicotine-induced chemoreceptor responses of the carotid body.

Animals↗
PubMed2004

The role of carotid chemoreceptors in the sympathetic activation by adenosine in humans.

The direct vasodilatory and negative chronotropic effects of adenosine in humans are counterbalanced by a reflex increase in sympathetic nerve traffic. A suggested mechanism for this reflex includes peripheral chemoreceptor activation. We, therefore, assessed the contribution of carotid chemoreceptors to sympatho-excitation by adenosine. Muscle sympathetic nerve activity was recorded during adenosine infusion (140 microg.kg(-1).min(-1) for 5 min) in five patients lacking carotid chemoreceptors after bilateral carotid body tumour resection (one male and four female, mean age 51 +/- 11 years) and in six healthy controls (two male and four female, mean age 50 +/- 7 years). Sympathetic responses to sodium nitroprusside injections were assessed to measure baroreceptor-mediated sympathetic activation. In response to adenosine, controls showed no change in blood pressure, an increase in heart rate (+48.2 +/- 13.2%; P<0.003) and an increase in sympathetic nerve activity (+195 +/- 103%; P<0.022). In contrast, patients showed a decrease in blood pressure (-14.6 +/- 4.9/-17.6 +/- 6.0%; P<0.05), an increase in heart rate (+25.3 +/- 8.4%; P<0.032) and no significant change in sympathetic activity. Adenosine-induced hypotension in individual patients elicited less sympathetic activation than equihypotensive sodium nitroprusside injections. In humans lacking carotid chemoreceptors, adenosine infusion elicits hypotension due to the absence of significant sympatho-excitation. Chemoreceptor activation is essential for counterbalancing the direct vasodilation by adenosine. In addition, blunting of the baroreflex sympathetic response to adenosine-induced hypotension may indicate a direct sympatho-inhibitory effect of adenosine.

Adenosine↗
PubMed1978

Nature of differential sympathetic discharges in chemoreceptor reflexes.

In a study of autonomic reflexes it was found that some produce a generalized, bilaterally uniform response whereas others have an asymmetric or laterality of action. Recordings from vertebral nerve fibers (mainly vasoconstrictors to forelimb muscles), right and left cardiac sympathetics, and renal nerves show that baroreceptors evoke a bilaterally uniform inhibition but chemoreceptors of the carotid sinus and aortic arch initiate a differential discharge. In the chemoreceptor reflex the vagi are activated and bradycardia generally occurs. Vertebral and renal sympathetic fibers increase their activity bilaterally commensurate with the increase in arterial pressure. Sympathetic discharges to the heart, however, are not uniform; they show ipsilateral inhibition and a strong contralateral increase in activity. Stabilization of blood pressure or inactivation of baroreceptors abolishes the ipsilateral inhibition. In isolation, therefore, the chemoreceptor-induced cardiac sympathetic discharge is just quantitatively stronger contralaterally. In the absence of vagi, heart rate changes differ depending on which chemoreceptors are stimulated, because the pacemaker is on the right. Asymmetrical discharges do occur and, in the eventual response to stimulation of chemoreceptors, reflex interactions actually augment the laterality of effects. Peripheral interactions, in the sense that changes effected by one may induce another reflex, are responsible in part for the balances of autonomic activity ultimately seen as the body reacts to stimuli.

Animals↗
PubMed1999

Chemoreceptor discharges and cytochrome redox changes of the rat carotid body: role of heme ligands.

In superfused in vitro rat carotid body, we recorded chemoreceptor discharges and the redox state of cytochromes simultaneously to identify the primary oxygen-sensing protein controlling transmitter release and electrical activity of the carotid sinus nerve. These parameters were tested under the influence of heme ligands such as oxygen, cyanide, 4-(2-aminoethyl)-benzenesulfonyl fluoride, and CO. During stimulation, there was an initial increase in discharge frequency followed by a decline or suppression of activity. Photometric changes lagged and were maintained as nerve activity decreased. Reducing mitochondrial cytochromes by cyanide or prolonged severe hypoxia, suppressed the chemoreceptor discharge. 4-(2-Aminoethyl)-benzenesulfonyl fluoride, a specific inhibitor of the phagocytic cytochrome b(558), also silenced the chemoreceptors after an initial excitation. CO increased the chemoreceptor discharge under normoxia, an effect inhibited by light, when the cytochromes were not reduced. When the discharges were depressed by severe hypoxia, exposure to light excited the chemoreceptors and the cytochromes were reduced. The rapidity of the chemosensory responses to light and lack of effect on dopamine release from type I cells led us to hypothesize that carotid body type I cells and the apposed nerve endings use different mechanisms for oxygen sensing: the nerve endings generate action potentials in association with membrane heme proteins whereas cytosolic heme proteins signal the redox state, releasing modulators or transmitters from type I cells.

Afferent Pathways↗
PubMed1997

Convergence of oropharyngolaryngeal, baroreceptor and chemoreceptor afferents onto insular cortex neurons in rats.

Forty-two neurons that responded to electrical stimulation of at least one of four nerves, the chorda tympani (CT), the lingual-tonsillar branch of the glossopharyngeal (LT-IXth) nerve, the pharyngeal branch of the glossopharyngeal (PH-IXth) nerve and the superior laryngeal (SL) nerve, were identified from the insular cortex by using glass microelectrodes in paralysed and anesthetized rats. Four, 42, 41 and 40 neurons responded to the CT, LT-IXth, PH-IXth and SL nerve stimulation respectively. Of these 42 neurons, most (37/42, 88.1%) responded to three nerves (the LT-IXth, PH-IXth and SL), two (4.8%) responded to two nerves and the remaining three (7.1%) responded to all four nerves. No neurons responded to one specific stimulus. The responsiveness of these 42 neurons to baroreceptor and chemoreceptor stimulation by an i.v. injection of three drugs was investigated. For baroreceptor stimulation, methoxamine hydrochloride (Mex) and sodium nitroprusside (SNP) were used; for chemoreceptor stimulation, sodium cyanide (NaCN) was used. Of the 42 neurons, 31 (73.8%) showed an excitatory or inhibitory response to baroreceptor and chemoreceptor stimulation with at least one of the three drugs, and the remaining 11 (26.2%) showed no response. Of these 31 baroreceptor and chemoreceptor-sensitive neurons, 19 (61.3%) responded to two or all three drugs, and the rest (12; 38.7%) responded to one. Most neurons recorded were distributed in the posterior insular cortex. These results indicate that the neurons in the posterior insular cortex receive convergent inputs from the oropharyngolaryngeal region, the baroreceptors and the chemoreceptors, suggesting that the posterior insular cortex may integrate various sensory information.

Animals↗
PubMed2003

Perception of noxious compounds by contact chemoreceptors of the blowfly, Phormia regina: putative role of an odorant-bindingpProtein.

The blowfly, Phormia regina, has sensilla with four contact-chemoreceptor cells and one mechanoreceptor cell on its labellum. Three of the four chemoreceptor cells are called the sugar, the salt and the water receptor cells, respectively. However, the specificity of the remaining chemoreceptor cell, traditionally called the "fifth cell", has not yet been clarified. Referring to behavioral evaluation of the oral toxicity of monoterpenes, we measured the electrophysiological response of the "fifth cell" to these compounds. Of all the monoterpenes examined, D-limonene exhibited the strongest oral toxicity and induced the severest aversive behavior with vomiting and/or excretion in the fly. D-Limonene, when dispersed in an aqueous stimulus solution including dimethyl sulfoxide or an odorant-binding protein (OBP) found in the contact-chemoreceptor sensillum, the chemical sense-related lipophilic ligand-binding protein (CRLBP), evoked impulses from the "fifth cell". Considering the relationship between the aversive effects of monoterpenes and the response of the "fifth cell" to these effects, we propose that the "fifth cell" is a warning cell that has been differentiated as a taste system for detecting and avoiding dangerous foods. Here we suggest that in the insect contact-chemoreceptor sensillum, CRLBP carries lipophilic members of the noxious taste substances to the "fifth cell" through the aqueous sensillum lymph. This insect OBP may functionally be analogous to the von Ebner's grand protein in taste organs of mammals.

Animals↗
PubMed2005

Retrotrapezoid nucleus: a litmus test for the identification of central chemoreceptors.

Central chemoreception is the mechanism by which arterial blood P(CO2) is detected by the CNS to regulate breathing. Two main theories have been proposed to account for the phenomenon. The distributed chemosensitivity theory argues that pH sensitivity is a widespread attribute of brainstem neurones and that central chemoreception results from the cumulative effects of pH on countless neurones. The specialized chemoreceptor theory envisions the existence of small and specialized populations of CNS cells (chemoreceptors) that are unique in their ability to detect very small pH fluctuations and, via specific connections, regulate a respiratory network that is itself unresponsive to pH. The recently identified CO2-sensitive neurones of the retrotrapezoid nucleus (RTN) seem to possess most of the attributes that one would expect of such chemoreceptors. In this review we also suggest that many fewer medullary neurones are intrinsically responsive to CO2 in vivo than might have been anticipated from prior experimentation in vitro. The properties of RTN neurones provide renewed support for the specialized chemoreceptor theory of central chemoreception, proposed in the early 1960s. However, many uncertainties remain, especially as regards the molecular mechanisms of chemoreception, the type of cell that actually detects pH in vivo (neurone, glia or others) and the number and location of bona fide central chemoreceptors.

Afferent Pathways↗
PubMed1969

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.

Animals↗
PubMed1970

The frequency of nerve impulses in single carotid body chemoreceptor afferent fibres recorded in vivo with intact circulation.

1. The responses of single afferent fibres of carotid body chemoreceptors to independent changes in arterial O(2) and CO(2) tensions and pH were studied in the cat in vivo.2. The response curve obtained relating chemoreceptor activity to changes in arterial P(O2) was similar to an hyperbola; the frequency of nerve impulses at first decreased rapidly as the P(a,O2) was raised and then more slowly. The arterial P(O2) at which the slow decrease was reached varied among the different fibres; the mean level was 190 mm Hg (S.D. +/- 40 mm Hg).3. Single chemoreceptor afferent fibres continued to discharge even when the arterial P(O2) was more than 600 mm Hg.4. The discharges of single chemoreceptor afferent fibres increased both with increasing P(a,CO2) at constant pH and P(a,O2), and with increasing arterial H(+) at constant P(a,CO2) and P(a,O2).5. It is concluded that single carotid body chemoreceptor afferent fibres of the cat can be activated in vivo by an increase in either arterial H(+) or arterial P(CO2) as well as by a decrease in arterial P(O2).

Action Potentials↗
PubMed1977

Respiratory modulation of baroreceptor and chemoreceptor reflexes affecting heart rate through the sympathetic nervous system.

1. Brief stimuli were delivered to the carotid body chemoreceptors or the carotid sinus baroreceptors at different phases of the respiratory cycle in anaesthetized dogs. Chemoreceptor stimulation was achieved by injecting small volumes (0.2-0.5 ml.) of warmed saline equilibrated with CO(2) near to the carotid bodies on both sides. Baroreceptor stimulation was achieved by injecting larger volumes (2-5 ml.) of saline equilibrated with air into the region of the carotid bifurcation on both sides, after first clamping the common carotid arteries.2. When the vagus nerves were intact, but sympathetic nervous effects on heart rate were blocked by administration of propranolol, there was a prompt and pronounced bradycardia evoked when either baroreceptor or chemoreceptor stimuli were given in expiration, but little or no change in heart rate when they were given in inspiration.3. When the vagus nerves were cut, but sympathetic nervous function was intact, respiratory modulation of both baroreceptor and chemoreceptor reflex effects on heart rate could still be demonstrated. The bradycardia evoked by either stimulus was more marked for stimuli given in expiration than for stimuli given in inspiration. A complementary response pattern for brief decreases in baroreceptor stimulation (carotid occlusions) was demonstrated: the tachycardia evoked by occlusions timed during inspiration was greater than that evoked by occlusions timed during expiration. All the reflex effects were mediated by the sympathetic system because they were abolished by administration of propranolol.4. Typically, the sympathetic reflex effects were slight in comparison with the vagal reflexes evoked by either chemoreceptor or baroreceptor stimuli.

Animals↗