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At least 199 records · Page 11Linked to original sources
PubMed1992

Carotid chemoreceptor discharge during epinephrine infusion in anesthetized cats.

It is known that during exercise there is an increase in plasma epinephrine. The purpose of the present investigation was to determine whether stimulation of carotid chemoreceptors by epinephrine is a direct effect or secondary to epinephrine-induced increases in arterial plasma [K+] and whole body CO2 production (VCO2). Chemoreceptor discharge was recorded from single fiber preparations of the carotid sinus nerves in anesthetized cats ventilated to a constant arterial PCO2 (PaCO2). Infusion of epinephrine (1 microgram.kg-1 x min-1) caused arterial [K+] to increase from a mean of 2.7 to 3.8 mM. VCO2 increased so that ventilation had to be increased by 60% to maintain PaCO2 constant. Mean chemoreceptor discharge increased by 50%, but this was no greater than would be predicted on the basis of the increases in arterial [K+] and VCO2. In a further group of experiments epinephrine was infused at 0.1 microgram.kg-1 x min-1 and produced no significant increase in chemoreceptor firing. These experiments provide no evidence for epinephrine having a direct effect on the carotid chemoreceptor.

Anesthesia, Intravenous↗
PubMed2005

Perinatal hyperoxia for 14 days increases nerve conduction time and the acute unitary response to hypoxia of rat carotid body chemoreceptors.

Hyperoxia in the immediate perinatal period, but not in adult life, is associated with a life-long impairment of the ventilatory response to acute hypoxia. This effect is attributed to a functional impairment of peripheral chemoreceptors, including a reduction in the number of chemoreceptor afferent fibers and a reduction in "whole nerve" afferent activity. The purpose of the present study was to assess the activity levels of single chemoreceptor units in the immediate posthyperoxic period to determine whether functional impairment extended to single chemoreceptor units and whether the impairment was only induced by hyperoxia exposure in the immediate postnatal period. Two groups of rat pups were exposed to 60% inspired O2 fraction for 2 wk at ages 0-14 days and 14-28 days, at which time single-unit activities were isolated and recorded in vitro. Compared with control pups, hyperoxia-treated pups had a 10-fold reduction in baseline (normoxia) spiking activity. Peak unit responses to 12, 5, and 0% O2 were reduced and nerve conduction time was significantly slower in both hyperoxia-treated groups compared with control groups. We conclude that 1) hyperoxia greatly reduces single-unit chemoreceptor activities during normoxia and acute hypoxia, 2) the treatment effect is not limited to the immediate newborn period, and 3) at least part of the impairment may be due to changes in the afferent axonal excitability.

Action Potentials↗
PubMed1997

Peripheral chemoreceptors in congenital central hypoventilation syndrome.

Congenital central hypoventilation syndrome (CCHS) is a rare disorder of unknown etiology, characterized by failure of the autonomic control of respiration. The primary defect is believed to involve central respiratory control; however, no specific lesion has been identified. We report two cases of CCHS (one female, 3 mo of age and one male 2 yr of age) in which there was detailed examination of the neural, muscular, and chemoreceptor components of respiratory control. Although no specific abnormalities were identified in the central nervous system (CNS) or muscles of respiration, striking changes were observed in arterial chemoreceptors, carotid bodies (CB), and airway chemoreceptors, neuroepithelial bodies (NEB). In both cases, CB were small (< 50% of control), with a marked decrease in the number of glomus cells identified by immunostaining for tyrosine hydroxylase and serotonin. Ultrastructural analysis of glomus cells in Case 1 showed a marked decrease in the frequency of dense core vesicles (< 20% of control), the storage site of amine and peptide neurotransmitters. Immunostaining for S100 protein, a marker of sustentacular or Type II cells, was increased up to twofold compared with controls. In the lung, the frequency and size of NEB immunostained for bombesin was increased twofold in both cases, suggesting compensatory hyperplasia of airway chemoreceptors. Since intact peripheral chemoreceptors are essential for respiratory control, especially the response to hypoxia, abnormalities in CB and NEB may contribute to the pathophysiology of CCHS and related conditions such as sudden infant death syndrome (SIDS).

Bombesin↗
PubMed1982

Localization of enkephalin-like immunoreactivity in the cat carotid and aortic body chemoreceptors.

The purpose of this study was to determine if enkephalin-like immunoreactivity was present in the glomus cells of the carotid and aortic body peripheral arterial chemoreceptors. Cat carotid and aortic bodies were reacted with antisera to met- and leu-enkephalin using the indirect peroxidase-antiperoxidase immunocytochemical method of Sternberger (1979). Both the carotid and aortic bodies demonstrated clusters of immunoreactive cells for both met- and leu-enkephalin. Additionally, met-enkephalin-like immunoreactivity was observed in many of the dense-core vesicles of the glomus cells of the carotid body. The glomus cells of these chemoreceptors are known to contain catecholamines which may modulate chemoreceptor activity. The presence of opioid peptide-like substances co-existing with the glomus cell catecholamines, perhaps in the same vesicles, may have important implications for a trophic influence of these peptides on glomus cell chemoreceptor modulation.

Animals↗
PubMed1978

Medullary and carotid chemoreceptor interaction for mild stimuli.

The interaction of medullary and carotid chemoreceptors during mild stimulation was investigated in 44 experiments on 6 chloralose-urethane anesthetized mongrel dogs using a donor-perfused, bilateral carotid sinus preparation. The donor dog breathed hypoxic mixtures (average PaO2 of 78 mm Hg) and the experimental animal breathed hypercapnic mixtures (average PACO2 of 49 mm Hg) in order to separately or simultaneously stimulate both chemoreceptor areas at low levels. After 4 min, the changes of tidal volume (VT), respiratory rate (f) and minute ventilation (VI), as a percentage of the control value, were compared to test whether the sums of the changes for separate stimuli were the same as for simultaneous stimuli, i.e. additive chemoreceptor effects. The simultaneous stimuli had significantly (P less than 0.05) greater responses for VT (19% greater than 5%) and VI (42% greater than 13%), but not for f (23% = 9%). Stepwise multiple regression studies of the response/control ratios on the blood gas values showed that multiplicative interaction terms accounted for more of the variance than additive terms for VT, f and VI and yielded equations which had overall significant slopes. We conclude that this evidence demonstrates that the two chemoreceptor effects combine synergistically at low levels of stimulation.

Animals↗
PubMedDate not supplied

Chemoreceptor drives and short sleep-wake cycles during hypoxia: a simulation study.

We used a Grodins-type mathematical model of the cardio-pulmonary system to investigate the cycling behaviour of the respiratory system during hypoxia in response to changes of state between waking and sleeping, namely a diminution of respiratory chemosensitivity during sleep. Shifts between waking and sleeping were triggered by various combinations of threshold values for PAO2. Mild or moderate hypoxia was simulated by values of inspired O2 concentration between 13% and 16% (normal 21%). In mild or moderate hypoxia, reductions of overall respiratory gain from about 2 to 0.8 l.min-1 mmHg-1 at sleep onset will produce falls in PAO2 likely to cause sleep-wake cycles with oscillations in PAO2. The higher the arousal threshold (in relation to steady-state PAO2 during sleep), the shorter and more stable the sleep-wake cycles. As the arousal threshold is raised, and as hypoxia is exacerbated from mild (FIO2 = 16%) to moderate (FIO2 = 13%), the sleep-wake cycle length tends to converge to a value around one minute. The level and determinants of the "back-to-sleep" threshold are hard to define from presently available experimental data, but the level is not important in determining the length of the sleep-wake cycle compared to the arousal threshold. Alinearities in chemoreceptor feedback were introduced first by incorporating "drive" thresholds, to simulate central or obstructive apnoea. This produced larger oscillations in respiratory variables, but no change in cycle length. Chemoreceptor thresholds for PCO2 at the level of 38-39 mmHg did produce shorter ventilation cycles, down to about 20 s in length, but these were not related in any simple way to the resulting sleep-wake cycles. The combination of sleep state changes and chemoreceptor feedback alinearities can produce short sleep-wake cycles despite the diminution in chemoreceptor gain occurring in sleep.

Chemoreceptor Cells↗
PubMed2000

Central projections from contact chemoreceptors of the locust ovipositor and adjacent cuticle.

Contact chemoreceptors (basiconic sensilla) located on the ovipositor and genital segments of the locust serve to control the chemical features of the substrate before and during oviposition. They occur dispersed and also crowded in fields between mechanosensory exteroceptors sensitive to touch or wind (trichoid and filiform sensilla). The central nervous projections of the four chemosensory and one mechanosensory neurons from single basiconic sensilla were stained selectively, focusing on receptors on the ovipositor valves, which usually contact the substrate during the pre-oviposition probing movements. All axons and neurites from one contact chemoreceptor usually stay close together in most of their projections. Segregation occurs mainly when single axons terminate in one neuromere while the others proceed to a different neuromere or ganglion. For projections from one chemoreceptor, there is evidence neither for functional segregation of mechanosensory from chemosensory afferent terminals nor for specific segregation between different chemosensory afferents. The projections from sensilla of dorsal cuticle tend to project rather uniformly along the midline of the terminal ganglion. Comparative staining of touch- and wind-sensitive hair receptor neurons shows mostly central projections, similar to those of neighbouring contact chemoreceptors. From the typical intersegmental projections of most primary afferents and from the lack of segregation into glomerular structures, we conclude that integration of chemosensory information from the genital segments is distributed in the terminal and the 7th abdominal ganglion.

Animals↗
PubMed1981

Hypercapnia and hypoxia: chemoreceptor-mediated control of locus coeruleus neurons and splanchnic, sympathetic nerves.

Utilizing single cell recording techniques to study brain norepinephrine (NE) neurons in the locus coeruleus (LC) and, in the same rats, registration of splanchnic nerve activity (SNA) the effects on these systems of hypercapnia and hypoxia, respectively, were studied. Hypercapnia (pCO2 36-103 mm Hg) caused a rapid increase in the firing rate of LC neurons as well as in SNA. This effect was directly correlated with the added amount of CO2 in the inspired gas mixture. This finding indicates a similar chemo-receptor-mediated regulation of LC neurons and SNA. Since deafferentation of peripheral chemoreceptors did not alter the response of these systems to hypercapnia, the chemoreceptors involved must be centrally located. In hypoxia (pO2 105-31 mm Hg) the overall effect on LC neurons was activation, whereas SNA was reduced. These effects were, however, not dose-dependent. Peripheral receptor deafferentation abolished the activation by hypoxia, suggesting that the LC neurons are influenced also by peripheral chemoreceptors. The results indicate that the previously observed increase in brain NE turnover in hypercapnia is largely secondary to increased neuronal activity and not due to, e.g., changes in metabolic enzymes. In addition, the data implicate chemoreceptors, centrally but also peripherally located, in the regulation of brain NE neurons in the LC. The activation of these neurons in hypercapnia, generally associated with increased apprehension in man, is consistent with the notion that the LC may serve as an alarm system in the brain.

Animals↗
PubMed1987

Effect of dopamine antagonism on carotid chemoreceptor interspike intervals.

As a means of examining the role of dopamine in chemotransduction, we examined the spike interval pattern from single carotid body chemoreceptors before and following dopamine antagonism. Before dopamine antagonism, chemoreceptor joint interval variability was less than the variability of the same spike interval series placed in shuffled order. This lower variability was abolished by dopamine antagonism with haloperidol. These data suggest that dopamine release reduces chemoreceptor interspike variability in vivo and that endogenous, local dopamine release is related to the activity level of a single chemoreceptor afferent.

Action Potentials↗
PubMed1975

Mechanisms of autonomic control of carotid chemoreceptor activity.

Single chemoreceptor fibres dissected from the cut carotid sinus nerves of cats were studied when carotid body blood flow was normal, and when it had been abruptly halted by reducing the local perfusion pressure to zero. Ten chemoreceptor fibres which, when normally supplied with blood, increased their discharge by at least 25% in response to sympathetic stimulation, and 7 fibres which, when normally supplied with blood, decreased their discharge by at least 10% in response to carotid sinus nerve stimulation, were chosen for study. The development of discharge during the period of stagnant asphyxia following stoppage of flow was reproducible in repeated control trials for each fibre investigated. Neither sympathetic nor carotid sinus nerve stimulation, commencing at the stoppage of flow and continued throughout the period of asphyxia, produced any significant alteration from the control pattern of developing chemoreceptor discharge. These experiments provide evidence that the effects of sympathetic and carotid sinus nerve stimulation on carotid chemoreceptor discharges are mediated through alterations in carotid body blood flow. When there is no flow there are no effects on discharge.

Animals↗
PubMed1978

Influence of the CSF bicarbonate concentration on the ventilatory response to CO2 in relation to the location of the central chemoreceptors.

In anaesthetized cats, in which the cerebrospinal fluid bicarbonate concentration was varied by a ventriculocisternal perfusion technique, the ventilatory response to CO2 during hyperoxia could be satisfactorily described by VE = S(PCSFCO2 -B). Both the slope S and the intercept B were positively and linearly related to the CSF bicarbonate concentration. Assuming that the PCSFCO2 is equal to the PCO2 in extracellular fluid, it can be shown that VE is a linear, but not a unique function of the [H+] at the site of the chemoreceptors; the slope of this relation varies with the bicarbonate concentration at that site, possibly due to chemical complex formation between HCO-3 and Ca2+ or Mg2+. Changes in the B-value were related to the location of the central chemoreceptors with the models of Pappenheimer and Berndt aand their coworkers. It was found that changes in the CSF bicarbonate concentration are reflected for 60 per cent at the site of the central chemoreceptors, and that this was independent of the cerebral perfusion. Using Berndt's model a distance between CSF and central chemoreceptors of approximately 100 micron was found; this calculated distance is relatively insensitive to relationship (logarithmic or not) between ventilation and H+ concentration and to changes in cerebral perfusion, owing to the approximate nature of the diffusion model.

Animals↗
PubMed1978

Avian intrapulmonary chemoreceptors: respiratory response to a step decrease in PCO2.

The contribution of intrapulmonary chemoreceptors (IPC) to the respiratory response, following a step decrease in PICO2 was assessed in anesthetized and unidirectionally ventilated chickens. Step changes in the PCO2 of the ventilatory gas (PICO2) to a single lung were introduced with PICO2 to the contralateral lung held constant. Respiratory amplitude and frequency were monitored. Experimental series were conducted under conditions such that (I) both systemic chemoreceptors and IPC, (II) systemic chemoreceptors alone and (III) IPC alone contribute to the ventilatory response. The results indicate (1) that a rapid component of the transient response (complete in 25 sec) is eliminated by sectioning the pulmonary nerves (Series II), and (2) within the rapid component, a localized minimum in respiratory amplitude was observed which was not seen in either Series II or Series III experiments. We conclude that the rapid component of the transient response is due to the CO2-sensitive IPC and that intrapulmonary and systemic chemoreceptors are not simply additive in the generation of respiratory amplitude and frequency, but a more complex interaction must be involved.

Animals↗
PubMed1984

Steady-state discharge and bursting of arterial chemoreceptors in the duck.

The steady-state discharge of fourteen arterial chemoreceptor preparations were recorded from the left cervical vagi of unidirectionally ventilated, pentobarbitone anaesthetized ducks. All were excited by both hypoxia and hypercapnia and these stimuli interacted multiplicatively, as they do in mammals. We located the receptive fields of three preparations by observing their responses to i.v. injections of 2,4-dinitrophenol before, during and after occlusion of various arteries. The responses of two preparations were consistent with their location in the ipsilateral carotid body, but the responses of one, containing two active fibres, suggested that its discharge originated in aortic bodies. The discharge of eleven preparations was not random, but came in short high frequency bursts. As stimulus intensity was increased by either hypoxia or hypercapnia the average number of impulses per burst decreased. We have shown that the arterial chemoreceptors of the duck are sensitive to both hypoxia and hypercapnia. Because the steady-state stimulus-response characteristics are essentially the same as those of mammals we suppose that both mammalian and avian chemoreceptors are excited by the same basic mechanism. We also show that ducks have active extra-carotid arterial chemoreceptors.

Animals↗
PubMed1992

Central chemoreceptor drive to breathing in unanesthetized toads, Bufo paracnemis.

Central chemoreceptor drive to breathing was studied in unanesthetized toads, equipped with face masks to measure pulmonary ventilation and arterial catheters to analyze blood gases. Two series of experiments were performed. Expt. 1: The fourth cerebral ventricle was perfused with solutions of mock CSF, adjusted to stepwise decreasing pH values. Concomitant perfusion-induced increases of pulmonary ventilation, pHa and PaO2 were measured. Expt. 2: Inspiration of hypercapnic gas mixtures was applied to stimulate both central and peripheral chemoreceptors. Subsequently, only peripheral chemoreceptors were stimulated. This was accomplished by repeating the hypercapnic conditions while the fourth ventricle was perfused with mock CSF at pH 7.7. This procedure reduced the slope of the ventilatory response curve by about 80%. Taken together, the experiments suggest a highly dominant role of central chemoreceptors in the ventilatory acid-base regulation of the toad.

Animals↗
PubMed1992

Avian arterial chemoreceptor responses to steps of CO2 and O2.

The responses of avian arterial chemoreceptor preparations to 44-sec steps of inspired CO2 and O2 were quantified. Anesthetized ducks were unidirectionally ventilated, arterial pH was recorded with a fast responding indwelling electrode, and neural activity was recorded from 28 preparations consisting of dissected filaments of the vagus nerve (23 single-fibered, 5 few-fibered). We analyzed responses using cycle-triggered stimulus histograms of neural discharge, cross correlation analysis, and analysis of variance. Average responses of the chemoreceptor preparations to PaCO2 steps from 24 +/- 1 to 38 +/- 1 Torr were larger (per Torr), occurred faster, and appeared more rate sensitive than the responses to PaO2 steps from 101 +/- 3 to 56 +/- 2 Torr. Average responses to CO2 steps usually appeared more rate sensitive when measured during arterial hypoxia than during arterial normoxia. These characteristics are very much like those reported for mammalian arterial chemoreceptors, except that responses of avian chemoreceptor preparations to repetitive CO2 steps were highly variable according to statistical analysis.

Animals↗
PubMed1993

Reflex carotid body chemoreceptor control of phrenic sympathetic neurons.

The reflex reaction of phrenic sympathetic neurons to stimulation of carotid body chemoreceptors was tested in chloralose-anesthetized and paralyzed cats with both vago-aortic nerves cut. During systemic hypoxia (animals ventilated with 10% O2 in N2) the sympathetic phrenic nerve activity increased from 100% in the control to 269%. This increase was markedly attenuated after cutting both sinus nerves. Reflex excitatory response in phrenic sympathetic neurons with the latency of 150 msec was evoked by electrical stimulation of the right carotid sinus nerve (3 pulses of 0.2 msec, 333 Hz). The central transmission time of the reflex was about 90 msec. Injecting 0.1 ml of 1 M NaHCO3 saturated with CO2 (in order to activate carotid body chemoreceptors) into the right or left carotid sinus, evoked excitatory responses in sympathetic neurons regardless of the side. The stimulation of carotid body chemoreceptors also increased somatic phrenic nerve activity. The three methods applied to the stimulation of carotid body chemoreceptors produced increase of phrenic nerve sympathetic activity.

Animals↗
PubMed1994

Chemoreceptors and control of episodic breathing in the bullfrog (Rana catesbeiana).

To test the hypothesis that the episodic breathing pattern of bullfrogs is necessarily caused by fluctuations of PaO2 and PaCO2/pH, the natural oscillations of blood gases associated with periods of ventilation and apnea were experimentally prevented by unidirectional ventilation (UDV) of lungs. UDV with air or a 50% O2 in N2 gas mixture eliminated breathing episodes; only sporadic single breaths were ever observed under these conditions. UDV with hypoxic or hypercarbic gas mixtures, however, produced episodic breathing despite the fact that UDV virtually eliminated fluctuations in pHa, PaCO2 and PaO2. Furthermore, the breathing patterns of animals with the same mean levels of blood gases and acid-base status, with (UDV) and without (non-UDV) phasic chemoreceptor input were identical. These data indicate that phasic chemoreceptor input plays little or no role in the control of the normal breathing pattern although some tonic level of chemoreceptor input is required for ventilation to occur. Animals on UDV were more sensitive to hypercarbic than hypoxic gases and hypoxemia and hypercapnia affected breathing pattern differently. This indicates that tonic chemoreceptor input also affects the length of the periods of apnea and ventilation but this must be through some mechanism other than an "on" or "off" threshold.

Animals↗
PubMed1987

Cat carotid body chemoreceptor responses before and after nicotine receptor blockade with alpha-bungarotoxin.

The nature of nicotine receptors in the carotid body was studied in anesthetized, paralyzed and artificially ventilated cats. Chemoreceptor discharge in single or few-fiber preparations of the carotid sinus nerve was measured during isocapnic hypoxia, hyperoxic hypercapnia and in response to nicotine injections before and after administration of alpha-bungarotoxin (10 cats) and after alpha-bungarotoxin plus mecamylamine (7 cats) which binds to neuromuscular-type nicotine cholinergic receptors. alpha-Bungarotoxin caused a slight enhancement of the chemoreceptor response to hypoxia without affecting the chemoreceptor stimulation by nicotine. Mecamylamine (1-5 mg, i.v.), a ganglionic-type nicotinic receptor blocker, had no further effect on the response to hypoxia while it completely abolished the chemoreceptor stimulation by nicotine. Thus the nicotinic receptors in the cat carotid body which elicit excitation of chemosensory fibers appear to be of the ganglionic-type. Blockade of neuromuscular and ganglionic types of nicotinic receptors in the carotid body by alpha-bungarotoxin and mecamylamine does not attenuate the chemosensory responses to either hypoxia or hypercapnia. These nicotinic receptors therefore, do not appear to play an essential role in hypoxic or hypercapnic chemoreception in the cat carotid body.

Action Potentials↗