Chemoreceptor responsiveness in fetal sheep

1992 ◽  
Vol 263 (1) ◽  
pp. H162-H167 ◽  
Author(s):  
P. F. Boekkooi ◽  
J. Baan ◽  
D. Teitel ◽  
A. M. Rudolph
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Arterial Occlusion ◽  
Peripheral Chemoreceptor ◽  
Fetal Sheep ◽  
Peripheral Chemoreceptors ◽  
Arterial Pco2 ◽  
Arterial O2 Saturation

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.

scholarly journals Intravenous adenosine and dyspnea in humans

2005 ◽  
Vol 98 (1) ◽  
pp. 180-185 ◽  
Author(s):  
Nausherwan K. Burki ◽  
Wheeler J. Dale ◽  
Lu-Yuan Lee
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Peripheral Chemoreceptor ◽  
C Fibers ◽  
Group Data ◽  
Lung Resistance ◽  
Time Latency ◽  
Stimulation Of

Intravenous adenosine for the treatment of supraventricular tachycardia is reported to cause bronchospasm and dyspnea and to increase ventilation in humans, but these effects have not been systematically studied. We therefore compared the effects of 10 mg of intravenous adenosine with placebo in 21 normal subjects under normoxic conditions and evaluated the temporal sequence of the effects of adenosine on ventilation, dyspnea, and heart rate. The study was repeated in 11 of these subjects during hyperoxia. In all subjects, adenosine resulted in the development of dyspnea, assessed by handgrip dynamometry, without any significant change ( P > 0.1) in lung resistance as measured by the interrupter technique. There were significant increases ( P < 0.05) in ventilation and heart rate in response to adenosine. The dyspneic response occurred slightly before the ventilatory or heart rate responses in every subject, but the timing of the dyspneic, ventilatory, and heart rate responses was not significantly different when the group data were analyzed (18.9 ± 5.8, 20.3 ± 5.5, and 19.7 ± 4.5 s, respectively). During hyperoxia, adenosine resulted in similar effects, with no significant differences in the magnitude of the ventilatory response; however, compared with the normoxic state, the intensity of the dyspneic response was significantly ( P < 0.05) reduced, whereas the heart rate response increased significantly ( P < 0.05). These data indicate that intravenous adenosine-induced dyspnea is not associated with bronchospasm in normal subjects. The time latency of the response indicates that the dyspnea is probably not a consequence of peripheral chemoreceptor or brain stem respiratory center stimulation, suggesting that it is most likely secondary to stimulation of receptors in the lungs, most likely vagal C fibers.

Electrocortical and heart rate response during vibroacoustic stimulation in fetal sheep

1997 ◽  
Vol 177 (1) ◽  
pp. 66-71 ◽  
Author(s):  
Reinhard Bauer ◽  
Matthias Schwab ◽  
Robert M. Abrams ◽  
Jana Stein ◽  
Kenneth J. Gerhardt
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Fetal Sheep

Reversal of hypoxia-induced decrease in human cardiac response to isoproterenol infusion

1989 ◽  
Vol 67 (2) ◽  
pp. 523-527 ◽  
Author(s):  
J. P. Richalet ◽  
J. L. Le-Trong ◽  
C. Rathat ◽  
P. Merlet ◽  
P. Bouissou ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sea Level ◽  
Heart Rate Response ◽  
Normal Values ◽  
Cardiac Response ◽  
Chronotropic Response ◽  
Beta Receptors ◽  
The Mean ◽  
Arterial O2 Saturation ◽  
Isoproterenol Infusion

A decrease in heart rate response to isoproterenol (IP) infusion has been previously described in humans exposed to acute (2–3 days) or chronic (21 days) exposure to altitude hypoxia (J. Appl. Physiol. 65: 1957–1961, 1988). To evaluate this cardiac response in subacute (8 days) hypoxia and to explore its reversal with restoration of normoxia, six subjects received an IP infusion under normoxia (condition N), after 8 days in altitude (4,350 m, condition H8), on the same day in altitude after inhalation of O2 restoring normoxic arterial O2 saturation (SaO2, condition HO), and 6–11 h (condition RN) and 4–5 mo (condition ND) after the return to sea level. Cardiac chronotropic response to IP, evaluated by the mean increase in heart rate from base value (delta HR, min-1), was lower in condition H8 [mean 30 +/- 13 (SD)] than in condition N (50 +/- 14, P less than 0.03); it was slightly higher in condition HO (38 +/- 14) or condition RN (42 +/- 15) than condition H8 but still significantly different from condition N (P less than 0.03), despite normal values of SaO2. delta HR in condition ND (55 +/- 10) returned to base N value. These findings confirm the hypothesis of a hypoxia-induced decrease in cardiac chronotropic function. Two possible mechanisms are suggested: an O2-dependent one, rapidly reversible with recent restoration of normoxia, and a more slowly reversible mechanism, probably a downregulation of the cardiac beta-receptors.

Peripheral chemoreceptor deactivation attenuates the sympathetic response to glucose ingestion

2019 ◽  
Vol 44 (4) ◽  
pp. 389-396 ◽  
Author(s):  
Megan P. Smorschok ◽  
Frances M. Sobierajski ◽  
Graeme M. Purdy ◽  
Laurel A. Riske ◽  
Stephen A. Busch ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Glucose ◽  
Animal Studies ◽  
Muscle Sympathetic Nerve Activity ◽  
Supplemental Oxygen ◽  
Burst Frequency ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Glucose Ingestion ◽  
Blood Glucose Concentrations

Acute increases in blood glucose are associated with heightened muscle sympathetic nerve activity (MSNA). Animal studies have implicated a role for peripheral chemoreceptors in this response, but this has not been examined in humans. Heart rate, cardiac output (CO), mean arterial pressure, total peripheral conductance, and blood glucose concentrations were collected in 11 participants. MSNA was recorded in a subset of 5 participants via microneurography. Participants came to the lab on 2 separate days (i.e., 1 control and 1 experimental day). On both days, participants ingested 75 g of glucose following baseline measurements. On the experimental day, participants breathed 100% oxygen for 3 min at baseline and again at 20, 40, and 60 min after glucose ingestion to deactivate peripheral chemoreceptors. Supplemental oxygen was not given to participants on the control day. There was a main effect of time on blood glucose (P < 0.001), heart rate (P < 0.001), CO (P < 0.001), sympathetic burst frequency (P < 0.001), burst incidence (P = 0.01), and total MSNA (P = 0.001) for both days. Blood glucose concentrations and burst frequency were positively correlated on the control day (r = 0.42; P = 0.03) and experimental day (r = 0.62; P = 0.003). There was a time × condition interaction (i.e., normoxia vs. hyperoxia) on burst frequency, in which hyperoxia significantly blunted burst frequency at 20 and 60 min after glucose ingestion only. Given that hyperoxia blunted burst frequency only during hyperglycemia, our results suggest that the peripheral chemoreceptors are involved in activating MSNA after glucose ingestion.

Prolonged apnea and impaired survival in piglets after sinus and aortic nerve section

1990 ◽  
Vol 68 (3) ◽  
pp. 1048-1052 ◽  
Author(s):  
D. F. Donnelly ◽  
G. G. Haddad
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Gases ◽  
Active Role ◽  
Nerve Section ◽  
Peripheral Chemoreceptors ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Aortic Nerve ◽  
Prolonged Apnea

We examined the effects of carotid body denervation (CX, n = 9), CX + aortic nerve section (CAX, n = 9), and sham surgery (SHAM, n = 7) on cardiorespiratory and metabolic function in young piglets (less than 9 days). For comparison, 1-mo-old pigs were also studied. Studies were performed 1 day after surgery, during which time ventilation (barometric plethysmography), heart rate, blood pressure, arterial blood gases, and electroencephalogram were recorded under normoxia. CX and CAX piglets hypoventilated (arterial PCO2 = 47.1 +/- 2.6 and 45.4 +/- 3.1 Torr, respectively) compared with SHAM piglets (arterial PCO2 = 36.4 +/- 1.5 Torr). CX piglets had an average of 8.0 +/- 3.0 apneas/h, lasting, on average, 26 +/- 3 s. CAX piglets averaged 17.2 +/- 7.9 apneas/h, lasting 30 +/- 5 s. Such long apneas were never observed in SHAM animals. Mean heart rate and blood pressure in denervated piglets were not significantly different from those in SHAM piglets. In animals followed up poststudy, significantly high mortality was observed in CX (5 of 9) and CAX (6 of 9) piglets by 7 days after surgery but not in SHAM animals (0 of 7) despite identical environmental and feed conditions (P less than 0.05; chi 2). One-month-old denervated animals showed periodic breathing and hypoventilation, but none died. These results suggest that in the newborn piglet 1) peripheral chemoreceptors have an active role in maintaining normal ventilation and avoidance of prolonged apnea and 2) survivability in early life is critically dependent on peripheral chemoreceptors.

Preservation of the Hypoxic Drive to Breathing in Diabetic Autonomic Neuropathy

1982 ◽  
Vol 63 (1) ◽  
pp. 17-22 ◽  
Author(s):  
P. M. A. Calverley ◽  
D. J. Ewing ◽  
I. W. Campbell ◽  
P. K. Wraith ◽  
H. M. Brash ◽  
...  
Keyword(s):  
Heart Rate ◽  
Autonomic Neuropathy ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Diabetic Autonomic Neuropathy ◽  
Co2 Production ◽  
Diabetic Patients ◽  
Normal Range ◽  
Peripheral Chemoreceptors ◽  
Carotid Chemoreceptors

1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia () during exercise in 22 male diabetic patients, six with symptomatic and cardiovascular evidence to suggest diabetic autonomic neuropathy (DAN+) and 12 without these features (DAN−). 3. There was no difference in the ventilatory response to transient hypoxia between the different groups of diabetic patients ( in DAN+ patients = −0·9 ± 0·2 litre min−1 kPa−1; in DAN− patients = −1·2 ± 0·6 litres min−1 kPa−1) even allowing for differences in the level of exercise achieved (CO2 production in DAN+ patients = 743 ± 103 ml/min; CO2 production in DAN– patients = 800 ± 144 ml/min). These results fell within our normal range for ventilatory response to transient hypoxia at this level of exercise. 4. The heart rate response to transient hypoxia varied within the groups but was significantly (P < 0·05) less in the patients with established diabetic autonomic neuropathy. 5. We conclude that the peripheral chemoreceptors are intact in diabetic autonomic neuropathy and that other mechanisms must be implicated in the unexpected cardiorespiratory arrests seen in these patients.

Mechanisms of improved arterial oxygenation after peripheral chemoreceptor stimulation during hypoxic exercise

1993 ◽  
Vol 74 (4) ◽  
pp. 1666-1671 ◽  
Author(s):  
R. Naeije ◽  
C. Melot ◽  
G. Niset ◽  
M. Delcroix ◽  
P. D. Wagner
Keyword(s):  
Minute Ventilation ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Peripheral Chemoreceptor ◽  
Pulmonary Hemodynamics ◽  
Arterial Pco2 ◽  
Fractional Concentration ◽  
Before And After ◽  
Arterial O2 Saturation ◽  
Hypoxic Exercise

Almitrine, a peripheral chemoreceptor agonist, has been reported to increase arterial O2 saturation (SaO2) without changing minute ventilation (VE) during hypoxic exercise (Giesbrecht et al. J. Appl. Physiol. 70: 1770–1774, 1991). To explain this finding, we studied pulmonary hemodynamics (right heart catheterization) and gas exchange (multiple inert gas elimination technique) in six healthy volunteers at rest and during heavy exercise in normobaric normoxia (fractional concentration of O2 in inspired air 0.21) or hypoxia (fractional concentration of O2 in inspired air 0.125), before and after 75 mg of almitrine taken orally. During normoxic exercise, at a mean O2 uptake (VO2) of 4.0 l/min, almitrine increased arterial PO2 (PaO2) (P < 0.05), SaO2 (P < 0.01), and VE (P < 0.05) and decreased arterial PCO2 (P < 0.01), without affecting pulmonary hemodynamics or ventilation-perfusion distributions. During hypoxic exercise, at a mean VO2 of 3.0 l/min, almitrine increased SaO2 (P < 0.01) and VE (P < 0.01) and decreased arterial PCO2 (P < 0.05), with no effect on PaO2 or on ventilation-perfusion distributions and with a slight pulmonary vasoconstriction (P < 0.01). Almitrine during hypoxia did not affect cardiac output or calculated O2 diffusing capacity, but it did increase the slope of the VE/VO2 relationship (P < 0.01). We conclude that during hypoxic exercise, a pharmacological stimulation of the peripheral chemoreceptors improves SaO2 but not PaO2 by means of increased ventilation and an associated leftward shift of the oxyhemoglobin dissociation curve.

Acidemia stimulates ACTH, vasopressin, and heart rate responses in fetal sheep

1989 ◽  
Vol 257 (2) ◽  
pp. R344-R349 ◽  
Author(s):  
C. E. Wood ◽  
H. G. Chen
Keyword(s):  
Heart Rate ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Highly Correlated

Adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and renin responses to hemorrhage are highly correlated to the hemorrhage-induced decreases in arterial pH. The present study was designed to test the responses of these three systems to acute fetal acidemia, produced by intravenous infusion of H+. HCl was infused into chronically catheterized fetal sheep at rates of 0.02 (n = 5), 0.10 (n = 6), and 0.50 (n = 5) meq/min. Infusions at rates of 0.10 and 0.50 meq/min significantly decreased fetal arterial pH and increased arterial PCO2. Fetal heart rate and plasma concentrations of ACTH, cortisol, and AVP were significantly increased during infusion of HCl at 0.5 meq/min. Neither fetal plasma renin activity nor fetal arterial blood pressure was significantly altered by any of the infusions. The results of these experiments suggest that fetal ACTH, AVP, and heart rate are stimulated by decreases in arterial pH and/or increases in arterial PCO2. We speculate that these responses are chemoreceptor mediated, although we cannot distinguish the apparent relative roles of peripheral and central chemoreceptors on the basis of the present study.

Chemoreceptor Reflexes in Preterm Infants: I. The Effect of Gestational and Postnatal Age on the Ventilatory Response to Inhalation of 100% and 15% Oxygen

PEDIATRICS ◽  
1975 ◽  
Vol 55 (5) ◽  
pp. 604-613
Author(s):  
Henrique Rigatto ◽  
June P. Brady ◽  
Rafael de la Torre Verduzco
Keyword(s):  
Heart Rate ◽  
Preterm Infant ◽  
Preterm Infants ◽  
Ventilatory Response ◽  
Periodic Breathing ◽  
Postnatal Life ◽  
Low Oxygen ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Oxygen Breathing

We studied 16 "healthy" preterm infants (birthweight, 1,000 to 2,000 gm) 94 times during postnatal life to define the effect of gestational and postnatal age on the ventilatory response to 100% and 15% oxygen. They were given air, then 100% oxygen for two and five minutes respectively (No. = 63) or 21%, 15%, and then 21% oxygen for five minutes each (No. = 31). We measured respiratory minute and tidal volumes, frequency, heart rate, and alveolar Pco2 and Po2. We used the magnitude of the immediate change in ventilation during 100% and 15% oxygen breathing to test peripheral chemoreceptor function. The immediate decrease in ventilation with 100% oxygen and the immediate increase in ventilation with 15% oxygen were statistically similar at different gestational and postnatal ages. The late increase in ventilation (five minutes) with 100% oxygen was also similar at different ages. However, the late decrease in ventilation with 15% oxygen was not present at 18 days of age. These findings suggest that: (1) the peripheral chemoreceptors are active at least from 28 weeks of gestation and are probably not important in triggering periodic breathing or apnea in preterm infants; and (2) the preterm infant matures his response to hypoxia and is able to sustain hyperventilation with low oxygen by 18 days of age.

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