Carotid body chemoreceptor reflexes and their interactions in the seal

1977 ◽  
Vol 232 (5) ◽  
pp. H517-H525 ◽  
Author(s):  
R. Elsner ◽  
J. E. Angell-James ◽  
M. de Burgh Daly
Keyword(s):  
Carotid Body ◽  
Superior Laryngeal Nerve ◽  
Harbor Seal ◽  
Minute Volume ◽  
Respiratory Response ◽  
Carotid Bodies ◽  
The Central Nervous System ◽  
Carotid Body Chemoreceptors ◽  
Spontaneously Breathing ◽  
Stimulation Of

In the anesthetized spontaneously breathing harbor seal Phoca vitulina stimulation of the carotid body chemoreceptors by intracarotid injections of sodium cyanide or by hypoxic hypercapnic blood causes an increase in tidal volume, respiratory frequency, and respiratory minute volume. The heart rate invariably decreased. Experimental dives caused apnea and bradycardia. When the carotid bodies are stimulated within 10 s of the commencement of a dive, the chemoreceptor-respiratory response is abolished, but the chemoreceptor-cardioinhibitory response is considerably enhanced. Electrical stimulation of the central cut end of a superior laryngeal nerve also causes apnea and bradycardia; stimulation of the carotid body now fails to produce a respiratory response but the cardioinhibitory effect is enhanced. These results indicate that the carotid bodies cause reflexly hyperventilation and bradycardia, and that these responses are considerably modified by other inputs to the central nervous system.

Cardiovascular-respiratory reflex interactions between carotid bodies and upper-airways receptors in the monkey

1978 ◽  
Vol 234 (3) ◽  
pp. H293-H299 ◽  
Author(s):  
M. B. Daly ◽  
P. I. Korner ◽  
J. E. Angell-James ◽  
J. R. Oliver
Keyword(s):  
Vascular Resistance ◽  
Pulmonary Ventilation ◽  
Superior Laryngeal Nerve ◽  
Macaque Monkey ◽  
Macaca Nemestrina ◽  
Upper Airways ◽  
Carotid Bodies ◽  
Spontaneously Breathing ◽  
Respiratory Stimulation ◽  
Stimulation Of

The carotid bodies were stimulated in the anesthetized pig-tailed macaque monkey (Macaca nemestrina) using i) brief injections of cyanide or CO2-equilibrated bicarbonate solution into a common carotid artery, and ii) longer perfusion with hypoxic hypercapnic blood in vascularly isolated chemoreceptor preparations. In spontaneously breathing animals, brief stimulations of the chemoreceptors consistently caused an increase in pulmonary ventilation, bradycardia, and an increase in femoral vascular resistance. When the same chemoreceptor stimulus was superimposed during the apneic period, reflexly evoked by stimulating either the central ends of the superior laryngeal nerves or the nasopharynx, the respiratory stimulation was absent or minimal, but the bradycardia and vasconstriction were greatly enhanced and exceeded the summed responses of separate stimulation of the chemoreceptors and one or the other of the upper-airways inputs. With sustained stimulation of the carotid bodies, hyperventilation, tachycardia, and femoral vasodilatation occurred due to overriding respiratory mechanisms. When superior laryngeal nerve stimulation was superimposed on this response, apnea occurred and tachycardia was reversed to bradycardia, and femoral vascular resistance increased above resting level. The interaction of autonomic responses resulting from chemoreceptor stimulation and from increases in the upper-airways inputs are qualitatively similar in the monkey and in subprimate species. Those involving specifically cardioinhibitory vagal responses are, in part at least, dependent on mechanisms related to the concomitant changes in respiration.

Chemical control of tracheal vascular resistance in dogs

1987 ◽  
Vol 63 (3) ◽  
pp. 988-995 ◽  
Author(s):  
G. Sahin ◽  
S. E. Webber ◽  
J. G. Widdicombe
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Carotid Body ◽  
Chemical Control ◽  
Artificial Ventilation ◽  
Systemic Hypoxia ◽  
Anesthetized Dogs ◽  
The Central Nervous System ◽  
Carotid Body Chemoreceptors ◽  
Stimulation Of

With anesthetized dogs we have measured upper tracheal vascular resistance on both sides of the trachea simultaneously by perfusing the cranial tracheal arteries and measuring inflow pressures at constant flows. The ratio of pressure to flow gave vascular resistance (Rtv). Lung airflow, blood pressure (BP), heart rate, and pressure in a cervical tracheal balloon (Ptr) were also measured. In paralyzed dogs, systemic hypoxia due to artificial ventilation with 10% O2–90% N2 increased Rtv by +8.1 +/- 1.0% (SE), Ptr by +76 +/- 22.8%, and BP by +18.9 +/- 24%. After bilateral cervical vagosympathectomy the increases in Rtv and BP were present (+8.8 +/- 0.9 and +22.3 +/- 0.3%, respectively). After carotid body denervation Rtv, Ptr, and BP increased (+6.4 +/- 1.3, +58.6 +/- 31.6, and +14.6 +/- 3.3%, respectively). After vagotomy Rtv and BP increased (+14.1 +/- 1.7 and +22.4 +/- 10.1%, respectively). Tracheal perfusion with hypoxic blood caused a small vasodilation (-2.2 +/- 1.1%). Systemic hypercapnia due to artificial ventilation with 8% CO2–92% air increased Rtv by +16.7 +/- 3.8%, Ptr by +67 +/- 2.0%, and BP by +12.9 +/- 9.9%. Tracheal perfusion with hypercapnic blood caused a small vasodilation (-2.5 +/- 1.2%). Stimulation of the carotid body chemoreceptors with KCN caused a small increase in Rtv (+1.2 +/- 0.5%) and increases in Ptr (+49.8 +/- 13.6%) and BP (+11.1 +/- 2.1%). Systemic hypoxia and hypercapnia caused tracheal vasoconstriction mainly by an action on the central nervous system.

Excitatory amino acid receptors in commissural nucleus of the NTS mediate carotid chemoreceptor responses

1993 ◽  
Vol 264 (1) ◽  
pp. R41-R50 ◽  
Author(s):  
A. Vardhan ◽  
A. Kachroo ◽  
H. N. Sapru
Keyword(s):  
Amino Acid ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Minute Ventilation ◽  
Neuronal Cell ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors ◽  
Neuronal Cell Bodies ◽  
Carotid Body Chemoreceptors ◽  
Stimulation Of

Stimulation of carotid body chemoreceptors by saline saturated with 100% CO2 elicited an increase in mean arterial pressure, respiratory rate, tidal volume, and minute ventilation (VE). Microinjections of L-glutamate into a midline area 0.5-0.75 mm caudal and 0.3-0.5 mm deep with respect to the calamus scriptorius increased VE. Histological examination showed that the site was located in the commissural nucleus of the nucleus tractus solitarii (NTS). The presence of excitatory amino acid receptors [N-methyl-D-aspartic acid (NMDA); kainate, quisqualate/alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and trans 1-amino-cyclopentane-trans-1,3-dicarboxylic acid (ACPD)] in this area was demonstrated by microinjections of appropriate agonists. Simultaneous blockade of NMDA and non-NMDA receptors by combined injections of DL-2-aminophosphonoheptanoate (AP-7; 1 nmol) and 6,7-dinitro-quinoxaline-2,3-dione (DNQX; 1 nmol) abolished the responses to stimulation of carotid body on either side. Combined injections of AP-7 and DNQX did not produce a nonspecific depression of neurons because the responses to another agonist, carbachol, remained unaltered. Inhibition of the neurons in the aforementioned area with microinjections of muscimol (which hyperpolarizes neuronal cell bodies but not fibers of passage) also abolished the responses to subsequent carotid body stimulation on either side.(ABSTRACT TRUNCATED AT 250 WORDS)

Excitatory amino acid receptors within NTS mediate arterial chemoreceptor reflexes in rats

1993 ◽  
Vol 265 (2) ◽  
pp. H770-H773 ◽  
Author(s):  
W. Zhang ◽  
S. W. Mifflin
Keyword(s):  
Electrical Stimulation ◽  
Amino Acid ◽  
Receptor Antagonist ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Pressor Responses ◽  
Carotid Body Chemoreceptors ◽  
Arterial Chemoreceptor ◽  
Stimulation Of ◽  
Arterial Baroreceptor

The nucleus tractus solitarius (NTS) is the primary site of termination of arterial baroreceptor and chemoreceptor afferent fibers. Excitatory amino acid (EAA) receptors within NTS have been shown to play an important role in the mediation of arterial baroreceptor reflexes; however, the importance of EAA receptors within NTS in the mediation of arterial chemoreceptor reflexes remains controversial. Therefore, in chloralose-urethan-anesthetized, mechanically ventilated, paralyzed rats, 4 nmol of the broad-spectrum EAA receptor antagonist kynurenic acid (Kyn) was injected into the NTS to observe the effects of EAA receptor blockade on the pressor responses evoked by either activation of ipsilateral carotid body chemoreceptors (by close arterial injection of CO2-saturated bicarbonate) or electrical stimulation of ipsilateral carotid sinus nerve (CSN). Under control conditions, activation of carotid body chemoreceptors and CSN stimulation evoked increases in arterial pressure of 27 +/- 2 (n = 24 sites) and 28 +/- 3% (n = 8), respectively. Kyn microinjection into NTS significantly reduced the pressor responses evoked by activation of carotid body chemoreceptors and electrical stimulation of the CSN for 20 and 25 min, respectively. Attenuation of pressor responses evoked by chemoreceptor activation were maximal at 20 min post-Kyn injection (13 +/- 2%), whereas CSN-evoked pressor responses were maximally attenuated at 15 min (6 +/- 4%). Microinjection into NTS of 4 nmol of xanthurenic acid, a structural analogue of Kyn with no EAA receptor antagonist properties, had no effect on chemoreceptor reflexes. We conclude that EAA receptors within NTS play an important role in the mediation of arterial chemoreceptor reflexes.

Fastigial nucleus-mediated respiratory responses depend on the medullary gigantocellular nucleus

2001 ◽  
Vol 91 (4) ◽  
pp. 1713-1722 ◽  
Author(s):  
Fadi Xu ◽  
Tongrong Zhou ◽  
Tonya Gibson ◽  
Donald T. Frazier
Keyword(s):  
Electrical Stimulation ◽  
Ibotenic Acid ◽  
Major Effect ◽  
Fastigial Nucleus ◽  
Respiratory Response ◽  
The Right ◽  
Spontaneously Breathing ◽  
Respiratory Responses ◽  
Gigantocellular Nucleus ◽  
Stimulation Of

Electrical stimulation of the rostral fastigial nucleus (FNr) alters respiration via activation of local neurons. We hypothesized that this FNr-mediated respiratory response was dependent on the integrity of the nucleus gigantocellularis of the medulla (NGC). Electrical stimulation of the FNr in 15 anesthetized and tracheotomized spontaneously breathing rats significantly altered ventilation by 35.2 ± 11.0% ( P < 0.01) with the major effect being excitatory (78%). This respiratory response did not significantly differ from control after lesions of the NGC via bilateral microinjection of kainic or ibotenic acid (4.5 ± 1.9%; P > 0.05) but persisted in sham controls. Eight other rats, in which horseradish peroxidase (HRP) solution was previously microinjected into the left NGC, served as nonstimulation controls or were exposed to either 15-min repeated electrical stimulation of the right FNr or hypercapnia for 90 min. Histochemical and immunocytochemical data showed that the right FNr contained clustered HRP-labeled neurons, most of which were double labeled with c-Fos immunoreactivity in both electrically and CO2-stimulated rats. We conclude that the NGC receives monosynaptic FNr inputs and is required for fully expressing FNr-mediated respiratory responses.

Reflex pulmonary vasoconstriction due to stimulation of the aortic body by nicotine

1964 ◽  
Vol 206 (6) ◽  
pp. 1189-1195 ◽  
Author(s):  
Shlomo Stern ◽  
Richard E. Ferguson ◽  
Elliot Rapaport
Keyword(s):  
Carotid Body ◽  
Control Period ◽  
Ascending Aorta ◽  
Sensory Receptors ◽  
Pulmonary Vasoconstriction ◽  
Vascular Beds ◽  
Carotid Body Chemoreceptors ◽  
The Right ◽  
Systemic Arteries ◽  
Stimulation Of

To study the hemodynamic effects of stimulation of the aortic and carotid body chemoreceptors, we injected 2.5– 20 µg/kg nicotine into the ascending aorta of anesthetized, artificially ventilated open-chest dogs. Pressures in the pulmonary artery, left atrium, and systemic arteries, and the stroke output of the right ventricle were measured simultaneously. Pulmonary and systemic vascular resistances (PVR, SVR) were calculated. Changes began 1.5–3.0 sec after the injection; the following two 5-sec periods were compared to a 5-sec control period immediately preceding injection. The injection of nicotine was followed by a significant reflex rise in PVR; the sensory receptors for the reflex were aortic chemoreceptors and the efferent paths were sympathetic fibers. Similar effects were not elicited by stimulation of the carotid body. Bronchoconstriction, changes in bronchial flow, shifts of blood volume between the vascular beds, and liberation of catecholamine were excluded as factors in the PVR increase. Bradycardia, increased SVR, and decreased flow also occurred after combined stimulation of the aortic and carotid chemoreceptors; however, when bradycardia was prevented by atropinization, no significant change in flow occurred.

The essential role of carotid body chemoreceptors in sleep apnea

2003 ◽  
Vol 81 (8) ◽  
pp. 774-779 ◽  
Author(s):  
Curtis A Smith ◽  
Hideaki Nakayama ◽  
Jerome A Dempsey
Keyword(s):  
Sleep Apnea ◽  
Carotid Body ◽  
Respiratory Acidosis ◽  
Periodic Breathing ◽  
Peripheral Chemoreceptors ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
The Difference ◽  
Carotid Body Chemoreceptors

Sleep apnea is attributable, in part, to an unstable ventilatory control system and specifically to a narrowed "CO2 reserve" (i.e., the difference in PaCO2 between eupnea and the apneic threshold). Findings from sleeping animal preparations with denervated carotid chemoreceptors or vascularly isolated, perfused carotid chemoreceptors demonstrate the critical importance of peripheral chemoreceptors to the ventilatory responses to dynamic changes in PaCO2. Specifically, (i) carotid body denervation prevented the apnea and periodic breathing that normally follow transient ventilatory overshoots; (ii) the CO2 reserve for peripheral chemoreceptors was about one half that for brain chemoreceptors; and (iii) hypocapnia isolated to the carotid chemoreceptors caused hypoventilation that persisted over time despite a concomitant, progressive brain respiratory acidosis. Observations in both humans and animals are cited to demonstrate the marked plasticity of the CO2 reserve and, therefore, the propensity for apneas and periodic breathing, in response to changing background ventilatory stimuli.Key words: sleep apnea, carotid bodies, hypocapnia, apneic threshold, periodic breathing.

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