Carotid chemoreceptor activity during acute and sustained hypoxia in goats

1988 ◽  
Vol 65 (4) ◽  
pp. 1796-1802 ◽  
Author(s):  
A. M. Nielsen ◽  
G. E. Bisgard ◽  
E. H. Vidruk
Keyword(s):  
Carotid Body ◽  
Discharge Frequency ◽  
Hypoxic Exposure ◽  
Arterial Pco2 ◽  
Afferent Discharge ◽  
Carotid Body Chemoreceptors ◽  
Arterial Po2 ◽  
Sustained Hypoxia ◽  
Related Increase

The role of carotid body chemoreceptors in ventilatory acclimatization to hypoxia, i.e., the progressive, time-dependent increase in ventilation during the first several hours or days of hypoxic exposure, is not well understood. The purpose of this investigation was to characterize the effects of acute and prolonged (up to 4 h) hypoxia on carotid body chemoreceptor discharge frequency in anesthetized goats. The goat was chosen for study because of its well-documented and rapid acclimatization to hypoxia. The response of the goat carotid body to acute progressive isocapnic hypoxia was similar to other species, i.e., a hyperbolic increase in discharge as arterial PO2 (PaO2) decreased. The response of 35 single chemoreceptor fibers to an isocapnic [arterial PCO2 (PaCO2) 38-40 Torr)] decrease in PaO2 of from 100 +/- 1.7 to 40.7 +/- 0.5 (SE) Torr was an increase in mean discharge frequency from 1.7 +/- 0.2 to 5.8 +/- 0.4 impulses. During sustained isocapnic steady-state hypoxia (PaO2 39.8 +/- 0.5 Torr, PaCO2, 38.4 +/- 0.4 Torr) chemoreceptor afferent discharge frequency remained constant for the first hour of hypoxic exposure. Thereafter, single-fiber chemoreceptor afferents exhibited a progressive, time-related increase in discharge (1.3 +/- 0.2 impulses.s-1.h-1, P less than 0.01) during sustained hypoxia of up to 4-h duration. These data suggest that increased carotid chemoreceptor activity contributes to ventilatory acclimatization to hypoxia.

Predominant role of peripheral chemoreceptors in the termination of apnea in maturing newborn lambs

1996 ◽  
Vol 80 (3) ◽  
pp. 892-898 ◽  
Author(s):  
C. Delacourt ◽  
E. Canet ◽  
M. A. Bureau
Keyword(s):  
Carotid Body ◽  
Pco2 Level ◽  
Peripheral Chemoreceptor ◽  
Arterial Pco2 ◽  
Postnatal Maturation ◽  
Body Function ◽  
Life Threatening ◽  
Prolonged Apnea ◽  
Arterial Po2

Apneas are very common and normal in newborns but may become life threatening if they are not terminated appropriately. The aim of this study in newborn lambs was to investigate the influence on apnea termination of postnatal maturation, peripheral chemoreceptor function, and hypoxia. Apneas were induced by passive hyperventilation at varying inspired O2 fraction levels. The apnea termination threshold PCO2 (PATTCO2) was defined as the arterial PCO2 value at the first breath after the apnea. Three groups of awake intubated lambs were studied: 1) intact lambs tested at both 1 and 15 days of life, 2) intact 1-day-old lambs with central tissue hypoxia induced by CO inhalation, and 3) 1-day-old lambs with carotid body denervation (CBD). In individual lambs and regardless of age and carotid body function, there was a PO2-PCO2 response curve that was a determinant for the termination of an apnea. PATTCO2 invariably increased when arterial PO2 increased, regardless of age. During hypoxia and normoxia, PATTCO2 was significantly lower in 15-day-old lambs compared with 1-day-old lambs. No difference was seen during hyperoxia. PATTCO2 values were shifted to higher levels after carotid body removal. Finally, hypoxia induced by either a low inspired O2 fraction or CO inhalation consistently failed to induce a depressive effect on the PATTCO2 even in CBD lambs. In conclusion, in awake newborn lambs, the PCO2 level for apnea termination changed with postnatal age, and carotid body function was essential in lowering PATTCO2, thus protecting the lambs against prolonged apnea. Furthermore, hypoxia consistently failed to depress the reinitiation of breathing after apnea, even in CBD lambs.

Adrenal response to long-term hypoxia is still increased after carotid body denervation in rat

1994 ◽  
Vol 76 (3) ◽  
pp. 1049-1054 ◽  
Author(s):  
Y. Dalmaz ◽  
J. M. Pequignot ◽  
J. M. Cottet-Emard ◽  
L. Peyrin
Keyword(s):  
Carotid Body ◽  
Normobaric Hypoxia ◽  
Hypoxic Exposure ◽  
Tyrosine Hydroxylation ◽  
Rat Adrenals ◽  
Adrenal Response ◽  
Carotid Body Chemoreceptors

This study investigated the effects of long-term normobaric hypoxia (10% O2 in N2 for 2, 7, 14, and 28 days) on the metabolism of catecholamines in rat adrenals and the role of the carotid body chemoreceptors in the adrenal response. The content and utilization of dopamine were significantly increased from the 7th day of hypoxia and remained enhanced thereafter. The content of norepinephrine and epinephrine decreased after 2 days of hypoxia and increased thereafter; after 28 days of hypoxia the norepinephrine amounts remained enhanced but the epinephrine levels were no longer significantly increased. In vivo tyrosine hydroxylation increased after 7 days of hypoxia. Bilateral transection of the carotid sinus nerve 1 wk before hypoxia failed to abolish the increase in the content and utilization of dopamine after 7, 14, or 21 days of hypoxic exposure. These results indicate that long-term normobaric hypoxia elicits a long-lasting increase in the metabolism of catecholamines in adrenals, especially as assessed by dopamine measurement, and that this response does not involve a carotid body chemoreflex pathway.

Role of carotid body chemoreceptors in cardiovascular adjustments induced by hypernatremia in rats

2011 ◽  
Vol 163 (1-2) ◽  
pp. 128
Author(s):  
G.R. Pedrino ◽  
M.V. Rossi ◽  
G.H.M. Schoorlemmer ◽  
O.U. Lopes ◽  
S.L.D. Cravo
Keyword(s):  
Carotid Body ◽  
Carotid Body Chemoreceptors

Hypoglycemia selectively abolishes hypoxic reactivity of pial arterioles in piglets: role of adenosine

1995 ◽  
Vol 268 (2) ◽  
pp. H871-H878 ◽  
Author(s):  
T. S. Park ◽  
E. R. Gonzales ◽  
A. R. Shah ◽  
J. M. Gidday
Keyword(s):  
Arterial Pco2 ◽  
Adenosine Receptor Antagonist ◽  
Cranial Window ◽  
Newborn Piglets ◽  
Window Technique ◽  
Pial Arterioles ◽  
Cerebrovascular Regulation ◽  
Arterial Po2 ◽  
Arteriolar Diameter

Episodes of hypoxia often occur in hypoglycemic newborns, but it is not known whether dysfunctions in cerebrovascular regulation contribute to brain injury incurred by these affected neonates. We tested the hypotheses that 1) perinatal hypoglycemia impairs cerebrovascular responses to hypoxia and 2) a reduced vascular smooth muscle sensitivity to adenosine accounts for this impairment. Responses of 25- to 50-mu m-diam pial arterioles were determined using the cranial window technique in isoflurane-anesthetized newborn piglets < 5 days of age. Hypoxia (arterial PO2 = 28 +/- 1 mmHg) caused a 47 +/- 5% increase (P = 0.0008) in arteriolar diameter, 89% of which could be blocked by prior superfusion of the window space with the preferential A2-adenosine receptor antagonist 3,7-dimethyl-1-propargylxanthine (DMPX; 50 microM). Insulin-induced hypoglycemia (blood glucose = 18 +/- 1 mg/dl without isoelectric electroencephalogram) caused a 31 +/- 5% increase (P = 0.002) in arteriolar diameter; however, no additional dilatative response to hypoxia (arterial PO2 = 28 +/- 1 mmHg) could be elicited in these animals. Arteriolar dilation of 41 +/- 6% (P = 0.002) induced by superfusion of 20 microM adenosine under normoglycemic conditions was also completely abolished after the animals were rendered hypoglycemic. Unlike the response to hypoxia and adenosine, hypoglycemia only attenuated prostanoid-dependent dilations to hypercapnia (arterial PCO2 = 68 +/- 3 mmHg) by 55 +/- 9%. These results indicate that, in the newborn, hypoglycemia selectively abolishes hypoxic reactivity through an impairment in adenosine-mediated cerebrovascular dilation.

Influence of reduced carotid body drive during sustained hypoxia on hypoxic depression of ventilation in humans

1996 ◽  
Vol 81 (2) ◽  
pp. 565-572 ◽  
Author(s):  
A. Dahan ◽  
D. Ward ◽  
M. van den Elsen ◽  
J. Temp ◽  
A. Berkenbosch
Keyword(s):  
Carotid Body ◽  
Hypoxic Exposure ◽  
Hypoxic Response ◽  
Air Breathing ◽  
Carotid Bodies ◽  
Delayed Recovery ◽  
End Tidal ◽  
Second Period ◽  
Sustained Hypoxia

To evaluate whether the intact hypoxic drive from the carotid bodies during sustained hypoxia is required for the generation of hypoxic depression of ventilation (VE), 16 volunteers were exposed to two consecutive periods of isocapnic hypoxia (first period 20 min; second period 5 min; end-tidal PO2 45 Torr) separated by 6 min of normoxia. In study A, saline was given. In study B, 3 micrograms.kg-1.min-1 i.v. dopamine (DA), a carotid body inhibitor, was given during the first hypoxic exposure followed by saline during normoxia and the second hypoxic exposure. In study C, 20 min of normoxia with DA preceded 6 min of normoxia and 5 min of hypoxia without DA. The first peak hypoxic VE (PHV) in study A was approximately 100% above normoxic VE. After 20 min of hypoxia, VE declined to 60% above normoxic VE. The second PHV in study A was only 60% of the first PHV. We relate this delayed recovery from hypoxia to "ongoing" effects of hypoxic depression. During DA infusion, the changes in VE due to sustained hypoxia were insignificant (study B). The second PHV in study B was not different from the PHV after air breathing in studies A and C. This indicates that the recovery from sustained hypoxia with a suppressed carotid body drive was complete within 6 min. Our results show that despite central hypoxia the absence of ventilatory changes during 20 min of isocapnic hypoxia due to intravenous DA prevented the generation of central hypoxic depression and the depression of a subsequent hypoxic response.

Role of ET-1 in hypoxia-induced mitosis of cultured rat carotid body chemoreceptors

Neuroreport ◽  
1999 ◽  
Vol 10 (18) ◽  
pp. 3739-3744 ◽  
Author(s):  
Mark Paciga ◽  
Cathy Vollmer ◽  
Colin Nurse
Keyword(s):  
Carotid Body ◽  
Carotid Body Chemoreceptors

ROLE OF CAROTID-BODY CHEMORECEPTORS AND THEIR REFLEX INTERACTIONS IN BRADYCARDIA AND CARDIAC ARREST

The Lancet ◽  
1979 ◽  
Vol 313 (8119) ◽  
pp. 764-767 ◽  
Author(s):  
M. De Burgh Daly ◽  
JenniferE. Angell-James ◽  
R. Elsner
Keyword(s):  
Cardiac Arrest ◽  
Carotid Body ◽  
Carotid Body Chemoreceptors
Sign in / Sign up

Export Citation Format

Share Document