Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chemoreceptor”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1983

Membrane properties of cat sensory neurones with chemoreceptor and baroreceptor endings.

The properties of chemoreceptor and baroreceptor neurones in the petrosal ganglion of the cat were examined in vitro with intracellular micro-electrodes. Chemoreceptor neurones with myelinated axons (average conduction velocity, 11 m/s) showed action potentials with a hump on the falling phase, followed by a prolonged after-hyperpolarization (average duration, 260 ms). The duration of the hump present in the action potential of chemoreceptor neurones was positively correlated with the duration of the after-hyperpolarization. In response to prolonged depolarization, chemoreceptor neurones showed only one or a few action potentials at the beginning of the depolarization. Two types of baroreceptors neurones with myelinated axons were found: fast (F) baroreceptors (average conduction velocity, 33 m/s) and slow (S) baroreceptors (average conduction velocity, 10 m/s). F baroreceptors had action potentials without a hump followed by a short after-hyperpolarization (average duration, 43 ms), while S baroreceptors had spikes similar to those found in chemoreceptors except for a shorter hyperpolarization (average duration, 145 ms). Both types of baroreceptor neurones fired repetitively throughout prolonged depolarization. It is concluded that, in the petrosal ganglion, primary sensory neurones originating a given type of sensory terminal share a particular set of electrophysiological properties.

Action Potentials↗
PubMed1988

Evidence for interaction between the contributions to ventilation from the central and peripheral chemoreceptors in man.

1. The question of whether there is any interaction between the peripheral and central chemoreceptor contributions to ventilation in man has been addressed. 2. Subjects were exposed to an end-tidal PCO2 of ca. 10 Torr above resting for 8 min at an end-tidal PO2 of 100 Torr. The end-tidal PCO2 was then reduced to near eucapnia. This provided a period of time when the PCO2 at the peripheral chemoreceptors would be near eucapnia, but would still be raised at the central chemoreceptors. 3. Against the background above, the effect of an hypoxic end-tidal step from a PO2 of 100 Torr to a PO2 of 50 Torr was studied, and compared with the effect of the same step when both sets of chemoreceptors were near eucapnia. 4. Three subjects were studied, each contributing twelve sets of data to each of the three protocols required for the comparisons. 5. In two of the three subjects, the ventilatory response to hypoxia was augmented when central PCO2 was high. 6. The results support the idea that there is an interaction between the central and peripheral chemoreceptors in man. The consequences of this and other possible interpretations of the results are discussed.

Adult↗
PubMed1991

The effect of discrete stimulation of carotid body chemoreceptors on atrial natriuretic peptide in anaesthetized dogs.

1. In seven chloralose-anaesthetized and artificially ventilated beagles, the carotid sinus regions were vascularly isolated and perfused with either arterial or mixed (arterial and venous) blood (PO2 46.4 +/- 1.5 mmHg, mean +/- S.E.M.) to stimulate the chemoreceptors at constant flow and pressure. Cervical vagosympathetic trunks were ligated in all dogs, and gallamine triethiodide (2.0 mg kg-1 h-1, I.V.) was given in five dogs. Right atrial pressure was measured in all dogs, and left atrial pressure in four dogs. Mean aortic pressure was held constant (91.0 +/- 3.0 mmHg) by means of a reservoir connected to the animal via the common carotid and femoral arteries. Plasma atrial natriuretic peptide (ANP) was measured by radioimmunoassay and urinary sodium by flame photometry. 2. In seven dogs with mean carotid sinus pressure maintained at 96.0 +/- 4.3 mmHg, stimulation of the carotid chemoreceptors for 25 min produced significant increases in left atrial pressure of 41.2 +/- 3.3% (n = 4; P less than 0.005) from 5.4 +/- 0.6 cmH2O and of 30.9 +/- 4.5% (n = 7; P less than 0.002) in ANP from 31.6 +/- 2.1 pg ml-1. However, chemoreceptor stimulation produced significant decreases in urine flow rate of 26.1 +/- 1.9% (n = 9; P less than 0.001) from 0.29 +/- 0.03 ml min-1 (100 g kidney weight)-1 and sodium excretion of 29.0 +/- 2.3% (P less than 0.001) from 8.5 +/- 1.7 mumol min-1 (100 g kidney weight)-1 but right atrial pressure and heart rate did not change significantly. In three of the dogs, beta-adrenoceptor blockade by atenolol (2 mg kg-1, I.V.) greatly reduced the effects of chemoreceptor stimulation on plasma levels of ANP. 3. The results show, for the first time, that discrete stimulation of the carotid chemoreceptors caused an increase in plasma ANP levels, probably due to the reflex increase in atrial pressure that results from an inhibition of the cardiac sympathetic nerves, and an increase in venous return from a reduction of peripheral vascular capacitance.

Anesthesia↗
PubMed1992

Primary effects of carotid chemoreceptor stimulation on gracilis muscle and renal blood flow and renal function in dogs.

1. In chloralose-anaesthetized and artificially ventilated dogs, the carotid sinus regions were vascularly isolated and perfused either with arterial or mixed (arterial and venous) blood (partial pressure of O2 (PO2) 43.8 +/- 2.4 mmHg, mean +/- S.E.M. n = 14) to stimulate the carotid chemoreceptors. The carotid sinus pressure was held constant at 142.0 +/- 2.8 mmHg. Measurements were made of renal and gracilis muscle blood flow by wrap-round electromagnetic flow probes placed around the renal and gracilis arteries, glomerular filtration rate by creatine clearance, urinary sodium excretion by flame photometry and solute excretion by osmometry. 2. In ten dogs, with intact cervical vagosympathetic trunks, carotid chemoreceptor stimulation produced significant increases in aortic pressure (AoP) of 12.7 +/- 1.1% (n = 10, P < 0.001), in glomerular filtration rate (GFR) of 14.7 +/- 4.1% (P < 0.001), urine flow rate (V) of 16.5 +/- 3.5% (P < 0.002), in urinary sodium excretion (UNaV) of 17.5 +/- 2.5% (P < 0.005) and in urinary osmolar excretion (UosmV) of 13.2 +/- 2.2% (P < 0.001), but a significant decrease in renal blood flow (RBF) of 5.8 +/- 1.8% (P < 0.02). In six of these dogs in which gracilis muscle blood flow (MBF) was also recorded, carotid chemoreceptor stimulation caused significant increases in AoP of 12.8 +/- 1.4% (n = 6, P < 0.001) and in MBF of 10.0 +/- 1.6% (P < 0.002), and a small but significant decrease in RBF of 3.6 +/- 1.5% (P < 0.02). 3. In fourteen dogs, with sectioned cervical vagosympathetic trunks, carotid chemoreceptor stimulation produced increases in AoP of 22.0 +/- 2.6% (n = 14, P < 0.001), in GFR of 36.9 +/- 4.2% (P < 0.001), in V of 30.1 +/- 4.4% (P < 0.001), in UNaV of 31.4 +/- 5.3% (P < 0.001), and in UosmV of 25.7 +/- 5.8% (P < 0.001). However, it produced a greater decrease in RBF of 10.5 +/- 1.9% (P < 0.001). In ten of these dogs, where MBF was recorded, carotid chemoreceptor stimulation caused greater increase in AoP of 22.4 +/- 3.0% (n = 10, P < 0.001) and in MBF of 32.8 +/- 3.7% (P < 0.001), and a greater decrease in RBF of 9.8 +/- 1.9% (P < 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Inspiratory drive and phase duration during carotid chemoreceptor stimulation in the cat: medullary neurone correlations.

1. This study addressed the hypothesis that there is a parallel processing of input from carotid chemoreceptors to brainstem neurones involved in inspiratory phase timing and control of inspiratory motor output amplitude. Data were from fifteen anaesthetized, bilaterally vagotomized, paralysed, artificially ventilated cats. Carotid chemoreceptors were stimulated by close arterial injection of 200 microliters of CO2-saturated saline solution. 2. Planar arrays of tungsten microelectrodes were used to monitor simultaneously up to twenty-two neurones in the nucleus tractus solitarii (NTS) and ventral respiratory group (VRG). Spike trains were analysed with two statistical tests of respiratory modulation, cycle-triggered histograms, peristimulus-time histograms, cumulative sum histograms and cross-correlograms. 3. In NTS, 16 of 26 neurones with respiratory and 12 of 27 without respiratory modulation changed firing rate during carotid chemoreceptor stimulation. In the VRG 72 of 112 respiratory and 14 of 48 non-respiratory neurones changed firing rate during stimulation. 4. The spike trains of 85 of 1276 pairs (6.7%) of cells exhibited short time scale correlations indicative of paucisynaptic interactions. Ten pairs of neurones were each composed of a rostral VRG phasic inspiratory neurone that responded to carotid chemoreceptor stimulation with a decline in firing rate and a caudal VRG phasic inspiratory neurone that increased its firing rate. Cross-correlograms from two of the pairs had features consistent with excitation of the caudal neurones by the rostral cells. A decrease in the duration of activity of the rostral VRG neurones was paralleled by the decrease in inspiratory time of phrenic nerve activity. Caudal VRG inspiratory neurones increased their activity as phrenic amplitude increased. Spike-triggered averages of all four neurones indicated post-spike facilitation of phrenic motoneurones. 5. The results support the hypothesis that unilateral stimulation of carotid chemoreceptors results in parallel actions. (a) Inhibition of rostral VRG I-Driver neurones decreases inspiratory duration. (b) Concurrent excitation of premotor VRG and dorsal respiratory group inspiratory neurones increases inspiratory drive to phrenic motoneurones. Other data suggest that responsive ipsilateral neurones act to regulate contralateral neurones.

Animals↗
PubMed1996

Reflex stimulation of aortic chemoreceptors through the stellate ganglion during hypoxia and hypotension in cats.

1. In cats anaesthetized with sodium pentobarbitone (35 mg kg-1), an investigation was made of the mechanisms underlying the enhancement of aortic chemoreceptor activity through the excitatory effect mediated by the sympathetic outflow to them during hypoxia and hypotension. 2. Removal of the right stellate ganglion significantly (P < 0.01) reduced the responses of the chemoreceptors to hypoxia and hypotension. Injection of a bolus of sodium pentobarbitone reduced the responses before, but not after, stellectomy. This indicated that the excitatory sympathetic influence on the chemoreceptors (attributed to glomeral vasoconstriction leading to reduction in blood flow) is exerted entirely through the right stellate ganglion. This excitatory effect was abolished after cutting the vagi and both carotid sinus nerves. 3. It is concluded that, in addition to the direct excitatory effect of hypoxia on aortic chemoreceptors, a reflex chemoreceptor excitatory component is mediated through the vagi, carotid sinus nerves and right stellate ganglion.

Animals↗
PubMed1997

Properties of ionic currents from isolated adult rat carotid body chemoreceptor cells: effect of hypoxia.

1. The electrical properties of chemoreceptor cells from neonatal rat and adult rabbit carotid bodies (CBs) are strikingly different. These differences have been suggested to be developmental and/or species related. To distinguish between the two possibilities, the whole-cell configuration of the patch-clamp technique was used to characterize the ionic currents present in isolated chemoreceptor cells from adult rat CBs. Since hypoxia-induced inhibition of O2-sensitive K+ currents is considered a crucial step in O2 chemoreception, the effect of hypoxia on the adult rat chemoreceptor cell currents was also studied. 2. Outward currents were carried mainly by K+, and two different components could be distinguished: a Ca(2+)-dependent K+ current (IK(Ca)) sensitive to Cd2+ and charybdotoxin (CTX), and a Ca(2+)-insensitive, voltage-dependent K+ current (IK(V)). IK(V) showed a slow voltage-dependent activation (time constant (tau) of 87.4 ms at -20 mV and 8.8 ms at +60 mV) and a very slow inactivation, described by the sum of two exponentials (tau 1 = 684 +/- 150 ms and tau 2 = 4.96 +/- 0.76 s at + 30 mV), that was almost voltage insensitive. The kinetic and pharmacological properties of IK(V) are typical of a delayed rectifier K+ channel. 3. Voltage-dependent Ca2+ currents (ICa) were present in nineteen of twenty-seven cells. TTX-sensitive Na+ currents were also observed in about 10% of the cells. 4. Low PO2 (< 10 mmHg) reduced the whole outward current amplitude by 22.17 +/- 1.96% (n = 27) at +20 mV. This effect was absent in the presence of Cd2+. Since low PO2 did not affect ICa, we conclude that hypoxia selectively blocks IK(Ca). 5. The properties of the currents recorded in adult rat chemoreceptor cells, including the specific inhibition of IK(Ca) by hypoxia, are similar to those reported in neonatal rat CB cells, implying that the differences between rat and rabbit chemoreceptor cells are species related.

Animals↗
PubMed1999

Clustering of the chemoreceptor complex in Escherichia coli is independent of the methyltransferase CheR and the methylesterase CheB.

The Escherichia coli chemoreceptors and their associated cytoplasmic proteins, CheA and CheW, cluster predominantly at the cell poles. The nature of the clustering remains a mystery. Recent studies suggest that CheR binding to and/or methylation of the chemoreceptors may play a role in chemoreceptor complex aggregation. In this study, we examined the intracellular distribution of the chemoreceptors by immunoelectron microscopy in strains lacking either the methyltransferase CheR or the methylesterase CheB. The localization data revealed that, in vivo, aggregation of the chemoreceptor complex was independent of either CheR or CheB.

Bacterial Proteins↗
PubMed2000

Intracellular Ca(2+) stores in chemoreceptor cells of the rabbit carotid body: significance for chemoreception.

The notion that intracellular Ca(2+) (Ca(i)(2+)) stores play a significant role in the chemoreception process in chemoreceptor cells of the carotid body (CB) appears in the literature in a recurrent manner. However, the structural identity of the Ca(2+) stores and their real significance in the function of chemoreceptor cells are unknown. To assess the functional significance of Ca(i)(2+) stores in chemoreceptor cells, we have monitored 1) the release of catecholamines (CA) from the cells using an in vitro preparation of intact rabbit CB and 2) the intracellular Ca(2+) concentration ([Ca(2+)](i)) using isolated chemoreceptor cells; both parameters were measured in the absence or the presence of agents interfering with the storage of Ca(2+). We found that threshold [Ca(2+)](i) for high extracellular K(+) (K(e)(+)) to elicit a release response is approximately 250 nM. Caffeine (10-40 mM), ryanodine (0.5 microM), thapsigargin (0.05-1 microM), and cyclopiazonic acid (10 microM) did not alter the basal or the stimulus (hypoxia, high K(e)(+))-induced release of CA. The same agents produced Ca(i)(2+) transients of amplitude below secretory threshold; ryanodine (0.5 microM), thapsigargin (1 microM), and cyclopiazonic acid (10 microM) did not alter the magnitude or time course of the Ca(i)(2+) responses elicited by high K(e)(+). Several potential activators of the phospholipase C system (bethanechol, ATP, and bradykinin), and thereby of inositol 1,4,5-trisphosphate receptors, produced minimal or no changes in [Ca(2+)](i) and did not affect the basal release of CA. It is concluded that, in the rabbit CB chemoreceptor cells, Ca(i)(2+) stores do not play a significant role in the instant-to-instant chemoreception process.

Animals↗
PubMed1992

Chemoreceptor responsiveness in fetal sheep.

Fetal peripheral chemoreceptor responses to arterial O2 saturation and changes in PCO2 have not yet been quantitated. In 24 late-term chronically instrumented fetal sheep, we measured the heart rate response to acute hypoxemia induced by uterine arterial occlusion at various resting O2 saturations (25-86%) and at induced reductions and increases in baseline O2 saturation. As an index of fetal chemoreceptor responsiveness we calculated the fall in heart rate divided by the fall in arterial O2 saturation (delta HR/delta sat). delta HR/delta sat was inversely related to resting O2 saturation at levels less than 65%, but greater than 65% this relationship was no longer present. However, an induced increase in baseline O2 saturation from 66 +/- 12 to 76 +/- 10% decreased delta HR/delta sat from 2.6 +/- 1.6 to 1.8 +/- 1.0, indicating that when resting O2 saturation is greater than 65% there may be adaptation of peripheral chemoreceptors. Below 65%, an induced decrease in baseline O2 saturation increased delta HR/delta sat (to 3.8 +/- 1.8), suggesting a lack of adaptation to lower O2 saturations. Concomitant changes in PCO2, or differences in baseline PCO2, did not affect delta HR/delta sat during uterine arterial occlusion, which suggests that there is no interdependence between O2 and CO2 as a stimulus for the fetal peripheral chemoreceptor. However, acute hypercapnia (n = 24 in 8 fetal sheep) induced bradycardia. Furthermore, this bradycardia was related to the increase in fetal arterial PCO2. We conclude that the fetal peripheral chemoreceptor is sensitive to hypoxemia and hypercapnia and that the hypoxemia response is accentuated with decreases in initial O2 saturation.

Acute Disease↗
PubMed1999

Contribution of carotid chemoreceptors to mesenteric venoconstriction during acute hypercapnia in rabbits.

The contribution of carotid chemoreceptors to hypercapnia-induced mesenteric venoconstriction was examined in 12 alpha-chloralose-anesthetized rabbits (1.0-1.6 kg). Surgical preparation consisted of a tracheotomy, femoral arterial and venous cannulation, and a midline laparotomy through which a 13-cm loop of ileum was exteriorized and superfused with physiological salt solution. Mesenteric vein diameter and intravenous pressure (using a servo-null measurement system) were measured in 500- to 1,000-micron mesenteric veins during 40-s periods of 15%, 20%, and 25% CO2 inhalation. Measurements were then repeated following bilateral ablation of the carotid chemoreceptors. Before denervation, mesenteric vein diameter constricted 6.5 +/- 1.1%, 11.9 +/- 1.1%, and 17.9 +/- 2.2% during the 15%, 20%, and 25% CO2 inhalation, respectively. After denervation, these values were reduced to 5.0 +/- 0.9%, 6.9 +/- 1.2%, and 8.4 +/- 1.3%, respectively. We conclude that activation of the carotid chemoreceptors by hypercapnia induces active mesenteric venoconstriction. After denervation of the carotid baroreceptors and chemoreceptors, there was also a small decrease in venule diameter proportional to the level of inspired CO2. We further conclude that noncarotid body chemoreceptor activation contributes to mesenteric venular constriction.

Animals↗
PubMed1995

Developmental changes in intracellular Ca2+ response of carotid chemoreceptor cells to hypoxia.

The carotid chemoreceptor response to hypoxia is weak just after birth and increases during postnatal development. The mechanisms underlying chemoreceptor maturation are unknown. We tested the hypothesis that carotid chemoreceptor maturation occurs at the glomus cell level by measuring intracellular calcium ([Ca2+]i) mobilization in response to hypoxia, anoxia, and NaCN in freshly dissociated cells from newborn vs. adult rabbit carotid bodies. Cells were loaded with fura 2 and superfused at 37 degrees C with balanced salt solution equilibrated with 5% CO2. [Ca2+]i mobilization in response to 3-min challenges of hypoxia (PO2 approximately 15 mmHg), anoxia (PO2 approximately 0 mmHg), and NaCN (1 mM) was measured using a digital imaging microscope. The fluorescence intensity ratio was used to calculate [Ca2+]i. Peak [Ca2+]i responses to all three challenges were three- to fivefold greater in glomus cells from adult compared with newborn carotid chemoreceptors. In addition, the average normoxic [Ca2+]i baseline was approximately threefold higher in the adult glomus cells. These results suggest that carotid chemoreceptor glomus cell sensitivity to natural stimuli, as reflected by the [Ca2+]i response, depends on the level of postnatal maturity.

Aging↗
PubMed1989

Chemoreceptor stimulation on sympathetic activity: dependence on respiratory phase.

Experiments were performed on chloralose-anesthetized, vagotomized, paralyzed, and artificially ventilated cats breathing 100% O2. Peripheral chemoreceptors were stimulated by rapid injections of CO2-saturated NaHCO3 in different phases of the respiratory cycle. Responses of cardiac and renal sympathetic nerves were computed by digital integration. Spontaneous sympathetic activity was consistently modulated by respiration, the modulation being greater for cardiac than for renal nerves. Cardiac nerve responses to peripheral chemoreceptor stimulation depended on the respiratory phase for at least one experimental condition in four of seven animals: the responses were largest during late inspiration and smallest (or absent) during postinspiration and early expiration. Renal nerve responses depended on respiratory phase in only two of eight animals. An average end-tidal CO2 concentration increase from 4.6 +/- 0.8% (SD) to 6.7 +/- 0.9% enhanced the respiratory modulation of spontaneous activity but reduced the responses to peripheral chemoreceptor stimulation. The results indicate that the respiratory modulation of chemoreceptor-induced sympathetic responses was less prominent than the modulation of spontaneous activity. It is hypothesized that the phase dependence of the responses is caused by the spontaneously occurring expiratory diminution of sympathetic activity rather than by an inherent gating of the chemoreceptor reflex.

Animals↗
PubMed1992

Arterial chemoreceptor input to nucleus tractus solitarius.

The arterial chemoreceptors play an important role in the reflex regulation of blood pressure and respiration. To investigate the initial integration of chemoreceptor inputs within the central nervous system, intracellular recordings were obtained in pentobarbital-anesthetized, paralyzed, and mechanically ventilated cats, from 58 cells within the nucleus of the tractus solitarius (NTS) that were depolarized by activation of the ipsilateral carotid body chemoreceptors. Close arterial injection of less than 100 microliters CO2-saturated bicarbonate evoked depolarizations of membrane potential with amplitudes of 2.2-4.6 mV and durations of 1.8-6.7 s in 46 cells. In 12 cells, activation of the carotid body chemoreceptors evoked a depolarization-hyperpolarization sequence. Electrical stimulation of the carotid sinus nerve (500 microA, 0.2 ms) evoked EPSPs [mean latency 6.4 +/- 0.5 (SE) ms; range 2.1-18.4 ms] in 46 cells and EPSP-IPSPs (7.3 +/- 0.8 ms; range 4.2-12.4 ms) in 12 cells. The distribution of EPSP latencies exhibited two peaks, one in the 2- to 4-ms range and another in the 7- to 8-ms range. Twenty-nine chemoreceptive cells were tested for the presence of convergent inputs from the ipsilateral carotid sinus baroreceptors. No evidence was found of a convergent postsynaptic inhibitory input from the baroreceptors within the NTS; however, seven cells were found that received an excitatory input from the baroreceptors. The observation that NTS neurons do not integrate chemoreceptor afferent inputs in a homogeneous manner suggests that the multiplicity of NTS unit responses might be related to the specific reflex function of an individual cell (e.g., vagal or sympathetic outflow, respiration).(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1993

Inhibition of chemoreceptor inputs to nucleus of tractus solitarius neurons during baroreceptor stimulation.

The reflex effects of arterial chemoreceptor activation are attenuated as arterial pressure is elevated and augmented as arterial pressure is decreased. This study was designed to test the hypothesis that excitatory arterial chemoreceptor inputs to neurons in the nucleus tractus solitarius (NTS) are inhibited by arterial baroreceptors. In pentobarbital sodium-anesthetized, mechanically ventilated, paralyzed cats, extracellular recordings were obtained from NTS neurons, which were excited after brief activation of ipsilateral carotid body chemoreceptors. During increases in arterial pressure, carotid sinus nerve (CSN)-evoked discharge was 45-112% of the control-evoked discharge at the prevailing level of arterial pressure (n = 70). Inhibition of CSN-evoked discharge during increased arterial pressure was significant when evoked discharge was < 90% of control (n = 31; 67 +/- 2%, mean percent of control-evoked discharge +/- SE; P < 0.01, Wilcoxon signed-rank test). The inhibition of CSN-evoked discharge was reduced after section of both vagi, both aortic nerves, and the contralateral CSN (n = 5, P < 0.05). These results demonstrate that activation of arterial baroreceptors attenuates excitatory chemoreceptor inputs to a subpopulation of NTS neurons. The inhibition appears to be mediated by disfacilitation. The results indicate that baroreceptor modulation of arterial chemoreflexes occurs at an early stage of the reflex arc, within the NTS. The results also suggest that sympathoinhibition evoked by baroreceptors might include, as a component, reduced sympathoexcitatory, i.e., chemoreceptor, drive.

Animals↗
PubMed1979

Aortic body chemoreceptor responses to changes in PCO2 and PO2 in the cat.

Responses of aortic chemoreceptor afferents to a range of arterial carbon dioxide tension (Paco2) changes at various levels of arterial oxygen tension (Pao2) were investigated in 18 cats anesthetized with alpha-chloralose and maintained at 38 degrees C. Aortic chemoreceptor activity, end-tidal oxygen pressure, end-tidal carbon dioxide pressure, and arterial blood pressure were continuously monitored. Arterial blood gases were measured in steady states. Single or a few clearly identifiable afferents were studied during changes and steady states of Pao2 and Paco2. All the aortic chemoreceptor afferent discharge rates increased with Paco2 increases from hypercapnia (10-15 Torr) to normocapnia and moderate hypercapnia (30-50 Torr) and with Pao2 decreases from above 400 to 30 Torr. Hypoxia augmented the response to Paco2 most effectively in the range of 10-40 Torr. At any Pao2, the discharge rate reached a plateau with sufficient intensity of hypercapnia. The Paco2 stimulus threshold at a Pao2 of 440 Torr was about 15 Torr, and at a Pao2 of 60 Torr it was 10 Torr. In the transition from hypocapnia to hypercapnia, responses increased gradually, usually without an overshoot. The steady-state responses to Paco2 of the majority of aortic chemoreceptors resembled those of carotid chemoreceptors. The responses of both receptors can be attributed to the same basic type of mechanism.

Animals↗
PubMed1980

Recovery of peripheral chemoreceptor function after denervation in ponies.

Resting ventilation (PaCO2) and ventilatory responses to acute hypoxia and to intravenous NaCN were assessed over a 4-yr period following cutting of the carotid sinus nerves and stripping the adventitia of the aortic arch. The data indicated essentially complete loss of peripheral chemoreceptor function immediately after surgery and hypoventilation during normoxia (delta PaCO2 = +8.7 Torr). There was a time-dependent, partial recovery of peripheral chemoreceptor function between 2 and 22 mo after surgery. Approximately 10% of the ventilatory response to iv NaCN returned, and 30-40% of the normal response to acute hypoxia was restored. Resting PaCO2 was no longer significantly elevated above normal by 22 mo after surgery. Four years after surgery these animals were unable to sustain normal ventilatory acclimatization to chronic hypoxia just as in an earlier study in the same ponies. Experiments carried out under anesthesia showed that recovered peripheral chemoreceptor sensitivity was not present in the carotid chemoreceptor area. However, sectioning of the aortic nerve caused the animals to again hypoventilate during acute hypoxia, and it nearly eliminated the ventilatory response to NaCN, but normal eucapnic ventilation was retained. We conclude that in the pony aortic chemoreceptors become functional in a time-dependent manner following carotid body denervation.

Acid-Base Equilibrium↗
PubMed1981

Effect of peripheral chemoreceptor denervation on acclimatization of goats during hypoxia.

The purpose of this study was to determine the effect of peripheral chemoreceptor denervation on ventilatory acclimatization of goats during chronic hypoxia. After 1 h of stimulated altitude (PB 450 Torr), arterial O2 tension (PaO2) in seven normal goats averaged 42 Torr, and arterial CO2 tension (PaCO2) was 1.3 Torr below control (P less than 0.001). In these goats nearly 66% of the increase in alveolar ventilation (VA) associated with acclimatization occurred between 1.5 and 4 h of hypoxia. Acclimatization was complete by the 3rd day of hypoxia, and it caused 1) a 23% increase in VA/CO2 output (P less than 0.001); 2) a 5-Torr increase in PaO2 (P less than 0.001); and 3) a 6.5-Torr decrease in PaCO2 (P less than 0.001). Denervation of the carotid chemoreceptors in seven goats caused hypoventilation during eupnea at sea level (PaCO2 change from control +7 Torr, P less than 0.001). Denervation also attenuated but did not eliminate peripheral chemoreceptor responsiveness. No additional changes were observed following attempted denervation of the aortic chemoreceptors. After 1 h of simulated altitude (PB 530 Torr), PaO2 in the denervated goats averaged 46 Torr, and PaCO2 was increased 1.1 Torr above control (P less than 0.001). In these goats VA did not change significantly during the subsequent 3 days of hypoxia. Accordingly, we conclude that the peripheral chemoreceptors are essential for ventilatory acclimatization of goats during chronic hypoxia.

Acclimatization↗