Early ultrastructural changes in the carotid body after degenerative section of the carotid sinus nerve in the cat

1972 ◽  
Vol 83 (2) ◽  
pp. 161-185 ◽  
Author(s):  
Carole P. Abbott ◽  
M. de Burgh Daly ◽  
A. Howe
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Ultrastructural Changes ◽  
Carotid Sinus Nerve

Respiratory responses to aortic and carotid chemoreceptor activation in the dog

1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku
Keyword(s):  
Electrical Stimulation ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Chemical Stimulation ◽  
Respiratory Drive ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Respiratory Reflexes ◽  
Respiratory Responses ◽  
Stimulation Of

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.

Neurotransmitter mechanisms in the carotid body: absence of ACh in the carotid sinus nerve

1978 ◽  
Vol 140 (2) ◽  
pp. 374-377 ◽  
Author(s):  
Alan M. Goldberg ◽  
Andrea P. Lentz ◽  
Roberts S. Fitzgerald
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve

Vagal inhibition of respiratory-linked efferent activity in the carotid sinus nerve

1984 ◽  
Vol 247 (4) ◽  
pp. R681-R686
Author(s):  
D. R. Kostreva ◽  
G. L. Palotas ◽  
J. P. Kampine
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Respiratory Rhythm ◽  
Systemic Blood Pressure ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Efferent Activity ◽  
Central Origin ◽  
Spontaneously Breathing

The hypothesis tested in this study was that glossopharyngeal efferent nerve activity coursing through the carotid sinus nerve has a central origin. Efferent activity in the carotid sinus nerve exhibited a respiratory rhythm in spontaneously breathing, closed-chest, mongrel dogs anesthetized with pentobarbital sodium (30 mg/kg iv). Carotid sinus nerve activity was recorded from the intact or cut central end of the carotid sinus nerve. Diaphragm electromyogram (D-EMG), carotid sinus pressure, systemic blood pressure, and electrocardiogram were also recorded. Before vagotomy, small increases in carotid sinus efferent nerve activity (CSENA) synchronous with increases in the D-EMG were observed during spontaneous inspiration. Section of the contralateral cervical vagosympathetic trunk markedly potentiated the increases in CSENA. Bilateral superior cervical ganglionectomy or nodose ganglionectomy failed to alter the increases in CSENA. Section of the ipsilateral glossopharyngeal nerve near the skull abolished the CSENA. This study demonstrates that respiratory-modulated glossopharyngeal efferents course through the carotid sinus nerve to the carotid sinus or carotid body. These efferents may be part of a central respiratory regulatory mechanism that may rapidly alter the sensitivity of the carotid sinus baroreceptors and/or carotid body receptors on a breath-to-breath basis.

Carbonic anhydrase in the carotid body and the carotid sinus nerve

1985 ◽  
Vol 82 (6) ◽  
pp. 577-580 ◽  
Author(s):  
R. Rigual ◽  
C. I�iguez ◽  
J. Carreres ◽  
C. Gonzalez
Keyword(s):  
Carbonic Anhydrase ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve

Postnatal maturation of carotid body and type I cell chemoreception in the rat

1999 ◽  
Vol 276 (5) ◽  
pp. L875-L884 ◽  
Author(s):  
Owen S. Bamford ◽  
Laura M. Sterni ◽  
Michael J. Wasicko ◽  
Marshall H. Montrose ◽  
John L. Carroll
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Type I ◽  
Carotid Sinus Nerve ◽  
Postnatal Maturation ◽  
Cell Responses ◽  
Type I Cells ◽  
Intracellular Ca ◽  
I Cells

The site of postnatal maturation of carotid body chemoreception is unclear. To test the hypothesis that maturation occurs synchronously in type I cells and the whole carotid body, the development of changes in the intracellular Ca2+ concentration responses to hypoxia, CO2, and combined challenges was studied with fluorescence microscopy in type I cells and compared with the development of carotid sinus nerve (CSN) responses recorded in vitro from term fetal to 3-wk animals. Type I cell responses to all challenges increased between 1 and 8 days and then remained constant, with no multiplicative O2-CO2interaction at any age. The CSN response to hypoxia also matured by 8 days, but CSN responses to CO2 did not change significantly with age. Multiplicative O2-CO2interaction occurred in the CSN response at 2–3 wk but not in younger groups. We conclude that type I cell maturation underlies maturation of the CSN response to hypoxia. However, because development of responses to CO2 and combined hypoxia-CO2 challenges differed between type I cells and the CSN, responses to these stimuli must mature at other, unidentified sites within the developing carotid body.

Dopamine, sensory discharge, and stimulus interaction with CO2 and O2 in cat carotid body

1998 ◽  
Vol 85 (5) ◽  
pp. 1719-1726 ◽  
Author(s):  
D. G. Buerk ◽  
S. Osanai ◽  
A. Mokashi ◽  
S. Lahiri
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Body Tissue ◽  
Initial Increase ◽  
Carotid Sinus Nerve ◽  
Bicarbonate Buffer ◽  
Flow Interruption ◽  
Carotid Bodies ◽  
Proportional Relationship ◽  
Baseline Values

It is hypothesized that carotid body chemosensory activity is coupled to neurosecretion. The purpose of this study was to examine whether there was a correspondence between carotid body tissue dopamine (DA) levels and neuronal discharge (ND) measured from the carotid sinus nerve of perfused cat carotid bodies and to characterize interaction between CO2 and O2 in these responses. ND and tissue DA were measured after changing from normoxic, normocapnic control bicarbonate buffer ([Formula: see text]>120 Torr, [Formula: see text] 25–30 Torr, pH ∼ 7.4) to normoxic hypercapnia ([Formula: see text] 55–57 Torr, pH 7.1–7.2) or to hypoxic solutions ([Formula: see text] 30–35 Torr) with normocapnia ([Formula: see text] 25–30 Torr, pH ∼ 7.4) or hypocapnia ([Formula: see text]10–15 Torr, pH 7.6–7.8). Similar temporal changes for ND and tissue DA were found for all of the stimuli, although there was a much different proportional relationship for normoxic hypercapnia. Both ND and DA increased above baseline values during flow interruption and normocapnic hypoxia, and both decreased below baseline values during hypoxic hypocapnia. In contrast, normoxic hypercapnia caused an initial increase in ND, from a baseline of 175 ± 12 (SE) to a peak of 593 ± 20 impulses/s within 4.6 ± 0.9 s, followed by adaptation, whereas ND declined to 423 ± 20 impulses/s after 1 min. Tissue DA initially increased from a baseline of 17.9 ± 1.2 μM to a peak of 23.2 ± 1.2 μM within 3.0 ± 0.7 s, then declined to 2.6 ± 1.0 μM. The substantial decrease in tissue DA during normoxic hypercapnia was not consistent with the parallel changes in DA with ND that were observed for hypoxic stimuli.

scholarly journals Dual effects of nitric oxide on cat carotid body chemoreception

2000 ◽  
Vol 89 (3) ◽  
pp. 1005-1012 ◽  
Author(s):  
Rodrigo Iturriaga ◽  
Sandra Villanueva ◽  
Matias Mosqueira
Keyword(s):  
Nitric Oxide ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Dependent Manner ◽  
Carotid Sinus Nerve ◽  
Dual Effect ◽  
No Donors ◽  
Pentobarbital Sodium ◽  
Carbon Fiber Microelectrodes ◽  
Dose Dependent

We studied the effects of nitric oxide (NO) released by NO donors on cat carotid body (CB) chemosensory activity during normoxia and hypoxia. CBs excised from pentobarbital sodium-anaesthetized cats were perfused with Tyrode at 38°C and pH 7.40. The frequency of chemosensory discharges (ƒx) was recorded from the carotid sinus nerve, and changes of NO concentration were measured by a chronoamperometric technique, with NO-selective carbon-fiber microelectrodes inserted in the CB. During steady chemosensory excitation induced by hypoxia, bolus injections of NO (ΔNO = 0.5–12 μM), released by S-nitroso- N-acetylpenicillamine (SNAP) and 6-(2-hydroxy-1-methyl-nitrosohydrazino)- N-methyl-1-hexanamine (NOC-9), transiently reduced ƒx in a dose-dependent manner. However, during normoxia, the same concentration of NO (ΔNO = 0.5–13 μM) released by the NO donors increased ƒx in a dose-dependent manner. The present results show a dual effect of NO on CB chemoreception that is dependent on the Po 2 levels. During hypoxia, NO is predominantly an inhibitor of chemoreception, whereas, in normoxia, NO increased ƒx. The mechanisms by which NO produces chemosensory excitation during normoxia remain to be determined.

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