Role of carotid chemoreceptors and pulmonary vagal afferents during helium-oxygen breathing in ponies

1987 ◽  
Vol 62 (3) ◽  
pp. 1020-1027 ◽  
Author(s):  
L. G. Pan ◽  
H. V. Forster ◽  
G. E. Bisgard ◽  
T. F. Lowry ◽  
C. L. Murphy
Keyword(s):  
Treadmill Exercise ◽  
Work Load ◽  
Vagal Afferents ◽  
Breathing Frequency ◽  
Heavy Exercise ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Oxygen Breathing ◽  
Carotid Bodies

Our purpose was to assess compensatory breathing responses to airway resistance unloading in ponies. We hypothesized that the carotid bodies and hilar nerve afferents, respectively, sense chemical and mechanical changes caused by unloading, hence carotid body-denervated (CBD) and hilar nerve-denervated ponies (HND) might demonstrate greater ventilatory responses when decreasing resistance. At rest and during treadmill exercise, resistance was transiently reduced approximately 40% in five normal, seven CBD, and five HND ponies by breathing gas of 79% He-21% O2 (He-O2). In all groups at rest, He-O2 breathing did not consistently change ventilation (VE), breathing frequency (f), tidal volume (VT), or arterial PCO2 (PaCO2) from room air-breathing levels. During treadmill exercise at 1.8 mph-5% grade in normal and HND ponies, He-O2 breathing did not change PaCO2 but at moderate (6 mph-5% grade), and heavy (8 mph-8% grade) work loads, absolute PaCO2 tended to decrease by 1 min of resistance unloading. delta PaCO2 calculated as room air minus He-O2 breathing levels at 1 min demonstrated significant changes in PaCO2 during exercise resistance unloading (P less than 0.05). No difference between normal and HND ponies was found in exercise delta PaCO2 responses (P greater than 0.10); however, in CBD ponies, the delta PaCO2 during unloading was greater at any given work load (P less than 0.05), suggesting finer regulation of PaCO2 in ponies with intact carotid bodies. During heavy exercise VE and f increased during He-O2 breathing in all three groups of ponies (P less than 0.05), although there were no significant differences between groups (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of chronic pulmonary denervation on ventilatory responses to exercise

1986 ◽  
Vol 61 (2) ◽  
pp. 603-610 ◽  
Author(s):  
P. S. Clifford ◽  
J. T. Litzow ◽  
J. H. von Colditz ◽  
R. L. Coon
Keyword(s):  
Treadmill Exercise ◽  
Minute Ventilation ◽  
Breathing Frequency ◽  
Inspiratory Time ◽  
Pressure Transducers ◽  
Ventilatory Responses ◽  
The Third ◽  
Exercise Challenge ◽  
Before And After

To assess the role of intrapulmonary receptors on the ventilatory responses to exercise we studied six beagle dogs before and after chronic pulmonary denervation and five dogs before and after sham thoracotomies. Each exercise challenge consisted of 6 min of treadmill exercise with measurements taken during the third minute at 3.2 km/h, 0% grade, and during the third minute at 5.0 km/h, 0% grade. Inspiratory and expiratory airflows were monitored with a low-dead-space latex mask and pneumotachographs coupled to differential pressure transducers. Both pre- and postsurgery, all dogs exhibited a significant arterial hypocapnia and alkalosis during exercise. Denervation of the lungs had no significant effect on minute ventilation at rest or during exercise, although there was a lower frequency and higher tidal volume in the lung-denervated dogs at all measurement periods. Breathing frequency increased significantly during exercise in lung-denervated dogs but to a lesser magnitude than in the control dogs. The changes that occurred in breathing frequency in all animals were due predominantly to the shortening of expiratory time. Inspiratory time did not shorten significantly during exercise following lung denervation. We conclude from these data that intrapulmonary receptors which are deafferented by sectioning the vagi at the hilum are not responsible for setting the level of ventilation during rest or exercise but are involved in determining the pattern of breathing.

Ventilatory control during exercise in calves with artificial hearts

1990 ◽  
Vol 68 (6) ◽  
pp. 2604-2611 ◽  
Author(s):  
A. Huszczuk ◽  
B. J. Whipp ◽  
T. D. Adams ◽  
A. G. Fisher ◽  
R. O. Crapo ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Treadmill Exercise ◽  
Ventilatory Control ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Output Increase ◽  
Exercise Hyperpnea ◽  
Artificial Hearts ◽  
Arterial Po2

To determine the role of cardiac reflexes in mediating exercise hyperpnea, we investigated ventilatory responses to treadmill exercise in seven calves with artificial hearts and seven controls. In both groups, the ventilatory responses were adequate for the metabolic demands of the exercise; this resulted in regulation of arterial PCO2 and pH despite the absence of cardiac output increase in the implanted group. In this group, there was a small but significant reduction of arterial PO2 by 4 +/- 3 Torr and a rise of blood lactate by 1.1 +/- 1 mmol/l. When cardiac output was experimentally increased in the implanted calves to a level commensurate with that spontaneously occurring in the control calves, ventilation was not affected. However, experimental reductions of cardiac output led to an immediate augmentation of exercise hyperpnea by 4.56 +/- 4.3 l/min and a further significant lactate increase of 1.2 +/- 1.22 mmol/l that was associated with a significant decrease in the exercise O2 consumption (0.32 +/- 0.13 l/min). These observations indicate that neither cardiac nor hemodynamic effects of increased cardiac output constitute an obligatory cause of exercise hyperpnea in the calf.

Carotid chemoreceptors in ventilatory responses to changes in venous CO2 load

1981 ◽  
Vol 51 (6) ◽  
pp. 1398-1403 ◽  
Author(s):  
E. A. Phillipson ◽  
G. Bowes ◽  
E. R. Townsend ◽  
J. Duffin ◽  
J. D. Cooper
Keyword(s):  
Ventilatory Response ◽  
Venous Blood ◽  
Major Influence ◽  
Arterial Pco2 ◽  
Peripheral Venous Blood ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Co2 Excretion

We examined the role of the carotid chemoreceptors in the ventilatory response to changes in venous CO2 load in 12 awake sheep using a venovenous extracorporeal perfusion circuit and two carbon dioxide membrane lungs (CDML). Three of the sheep had undergone surgical denervation of the carotid bodies (CBD). In the nine intact sheep, as CO2 was removed from or added to the peripheral venous blood through the CDML under normoxic conditions, there was a linear relationship between the rate of pulmonary CO2 excretion (VCO2) and the resulting rate of ventilation over a VCO2 range of 0--800% of control, so that arterial PCO2 remained close to isocapnic. In contrast, in the three CBD sheep, the ventilatory response to changes in VCO2 was significantly decreased under normoxic conditions, resulting in marked hypercapnia. The results indicate that the carotid chemoreceptors exert a major influence on the ventilatory response to changes in venous CO2 load.

Role of vagal afferents and the carotid bodies in the hypopnea consequent to diminished pulmonary blood flow

CHEST Journal ◽  
1978 ◽  
Vol 73 (2) ◽  
pp. 270b-272
Author(s):  
R. Stremel ◽  
B. Whipp ◽  
R Casaburi ◽  
D. Huntsman ◽  
K Wasserman
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Vagal Afferents ◽  
Carotid Bodies

Changes in breathing when switching from nares to tracheostomy breathing in awake ponies

1985 ◽  
Vol 59 (4) ◽  
pp. 1214-1221 ◽  
Author(s):  
H. V. Forster ◽  
L. G. Pan ◽  
G. E. Bisgard ◽  
C. Flynn ◽  
R. E. Hoffer
Keyword(s):  
Pulmonary Ventilation ◽  
Alveolar Ventilation ◽  
Breathing Frequency ◽  
Collection System ◽  
Heavy Exercise ◽  
Arterial Pco2 ◽  
Physiological Dead Space ◽  
Control Tube ◽  
Lung Resistance ◽  
System F

We assessed the consequences of respiratory unloading associated with tracheostomy breathing (TBr). Three normal and three carotid body-denervated (CBD) ponies were prepared with chronic tracheostomies that at rest reduced physiological dead space (VD) from 483 +/- 60 to 255 +/- 30 ml and lung resistance from 1.5 +/- 0.14 to 0.5 +/- 0.07 cmH2O . l-1 . s. At rest and during steady-state mild-to-heavy exercise arterial PCO2 (PaCO2) was approximately 1 Torr higher during nares breathing (NBr) than during TBr. Pulmonary ventilation and tidal volume (VT) were greater and alveolar ventilation was less during NBr than TBr. Breathing frequency (f) did not differ between NBr and TBr at rest, but f during exercise was greater during TBr than during NBr. These responses did not differ between normal and CBD ponies. We also assessed the consequences of increasing external VD (300 ml) and resistance (R, 0.3 cmH2O . l-1 . s) by breathing through a tube. At rest and during mild exercise tube breathing caused PaCO2 to transiently increase 2–3 Torr, but 3–5 min later PaCO2 usually was within 1 Torr of control. Tube breathing did not cause f to change. When external R was increased 1 cmH2O . l-1 . s by breathing through a conventional air collection system, f did not change at rest, but during exercise f was lower than during unencumbered breathing. These responses did not differ between normal, CBD, and hilar nerve-denervated ponies, and they did not differ when external VD or R were added at either the nares or tracheostomy.

Role of Vagal Afferents and the Carotid Bodies in the Hypopnea Consequent to Diminished Pulmonary Blood Flow

CHEST Journal ◽  
1978 ◽  
Vol 73 (2) ◽  
pp. 270-272 ◽  
Author(s):  
Richard W. Stremel ◽  
Brian J. Whipp ◽  
Richard Casaburi ◽  
David J. Huntsman ◽  
Karlman Wasserman
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Vagal Afferents ◽  
Carotid Bodies

Chemical and nonchemical components of ventilation during hypercapnic exercise in man

1980 ◽  
Vol 48 (6) ◽  
pp. 1065-1076 ◽  
Author(s):  
J. M. Clark ◽  
R. D. Sinclair ◽  
J. B. Lenox
Keyword(s):  
Similar Pattern ◽  
Treadmill Exercise ◽  
Ventilatory Response ◽  
Work Load ◽  
Heavy Exercise ◽  
Progressive Reduction ◽  
Young Athletes ◽  
Simple Addition ◽  
Average Slope ◽  
Exercise Hyperpnea

Nine young athletes performed treadmill exercise at average VO2 levels of 1.08, 1.78, 3.00, and 3.57 l/min while exposed to inspired PCO2 levels of 0, 10, 20, 30, and 40 Torr. The average slope of the VE-PACO2 relationship increased significantly from 3.59 to 4.70 l.min-1.Torr-1 in the transition from rest to light exercise and then decreased progressively and significantly to 1.34 l.min-1.Torr-1 at the highest work load. A similar pattern of initial increased steepness followed by progressive flattening was found in the VT-PACO2, curves, whereas slopes of the f-PACO2 relationships continuously decreased in the transition from rest through light to heavy exercise. These data are consistent both with an increased ventilatory response to PACO2--[H+]a increments during light exercise and with progressive reduction of that response during the transition from light to heavy exercise in parallel with increasingly severe mechanical influences on VE as maximal limits are approached. They are not consistent with simple addition of chemical and nonchemical components of exercise hyperpnea at all levels of exercise.

Role of VCO2 in control of breathing of awake exercising dogs

1984 ◽  
Vol 56 (5) ◽  
pp. 1335-1339 ◽  
Author(s):  
F. M. Bennett ◽  
R. D. Tallman ◽  
F. S. Grodins
Keyword(s):  
Directional Statistics ◽  
Direct Signal ◽  
Arterial Pco2 ◽  
Average Decrease ◽  
Ventilatory Responses ◽  
Co2 Output ◽  
Exercise Hyperpnea ◽  
Co2 Flow ◽  
End Tidal

Steady-state ventilatory responses to CO2 inhalation, intravenous CO2 loading (loading), and intravenous CO2 unloading (unloading) were measured in chronic awake dogs while they exercised on an air-conditioned treadmill at 3 mph and 0% grade. End-tidal PO2 was maintained at control levels by manipulation of inspired gas. Responses obtained in three dogs demonstrated that the response to CO2 loading [average increase in CO2 output (Vco2) of 216 ml/min or 35%] was a hypercapnic hyperpnea in every instance. Also, the response to CO2 unloading [average decrease in Vco2 of 90 ml/min or 15% decrease] was a hypocapnic hypopnea in every case. Also, the analysis of the data by directional statistics indicates that there was no difference in the slopes of the responses (change in expiratory ventilation divided by change in arterial Pco2) for loading, unloading, and inhalation. These results indicate that the increased CO2 flow to the lung that occurs in exercise does not provide a direct signal to the respiratory controller that accounts for the exercise hyperpnea. Therefore, other mechanisms must be important in the regulation of ventilation during exercise.

Role of hilar nerve afferents in hyperpnea of exercise

1985 ◽  
Vol 59 (3) ◽  
pp. 798-806 ◽  
Author(s):  
C. Flynn ◽  
H. V. Forster ◽  
L. G. Pan ◽  
G. E. Bisgard
Keyword(s):  
Minute Ventilation ◽  
Blood Gases ◽  
Vagal Afferents ◽  
Vagus Nerves ◽  
Inspiratory Time ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Cervical Vagotomy

The objective of this study was to determine the role of hilar nerve (lung vagal) afferents in the hyperpnea of exercise. Ten ponies were studied before and 2–4 wk and 3–12 mo after sectioning only the hilar branches of the vagus nerves (HND). After HND, lung volume feedback to the medullary centers was attenuated as indicated in the anesthetized state by 1) attenuation or absence of the Hering-Breuer inflation reflex (P less than 0.01) and 2) attenuation of the lengthened inspiratory time (TI) when the airway was occluded at end expiration (P less than 0.01). Moreover, after HND in the awake state, there was an increase in the ratio of TI to total cycle time (P less than 0.01). These changes verify a compromise in lung innervation comparable to cervical vagotomy. Resting arterial PCO2, PO2, and pH were not altered following HND (P greater than 0.10). Moreover, at three levels of mild and moderate treadmill exercise, no difference in either the temporal pattern or the absolute levels of arterial blood gases and arterial pH was found between pre- and post-HND studies (P greater than 0.10). In addition, minute ventilation (VE) at rest and during exercise was not altered by HND (P greater than 0.10). However, 2–4 wk after HND the increase in breathing frequency (f) during exercise was less, whereas the increase in tidal volume during exercise was greater than pre-HND (P less than 0.05). The reduced f was due to an increase in TI with no change in expiratory time. We conclude that lung afferents via the hilar nerves influence the pattern of breathing at rest and during exercise in ponies.

Ventilatory responses to lung inflation and arterial CO2 in halothane-anesthetized dogs

1988 ◽  
Vol 64 (4) ◽  
pp. 1433-1438 ◽  
Author(s):  
G. S. Mitchell ◽  
B. D. Selby
Keyword(s):  
Left Lung ◽  
Surgical Removal ◽  
Halothane Anesthesia ◽  
Burst Frequency ◽  
Lung Inflation ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Anesthetized Dogs ◽  
The Right

Hypercapnia attenuates the effects of static airway pressure (Paw) on phrenic burst frequency (f) and the expiratory duration (TE) in chloralose-urethan-anesthetized dogs. Surgical removal of the carotid bodies abolishes this interaction. Since halothane anesthesia in hyperoxia greatly impairs peripheral chemoreflexes, experiments were conducted to determine whether hypercapnia would attenuate the effects of Paw on f and TE in halothane-anesthetized dogs (approximately 1.5 minimum alveolar concentration). Integrated activity of the phrenic nerve was monitored as a function of Paw (2-12 cmH2O) in a vascularly isolated left lung at varied levels of arterial PCO2 (PaCO2; 38-80 Torr) controlled by inspired gas concentrations ventilating the denervated but perfused right lung. Halothane was administered only to the right lung. The results were as follows: 1) integrated phrenic amplitude increased with PaCO2 but was unaffected by Paw; 2) f decreased as Paw increased but was not affected by PaCO2; 3) the inspiratory duration (TI) increased as PaCO2 increased but was unaffected by Paw; 4) TE increased as Paw increased but was unaffected by PaCO2; and 5) there was no phrenic response to intravenous sodium cyanide (50-100 micrograms/kg). Thus, unlike chloralose-urethan-anesthetized dogs, hypercapnia does not attenuate the effect of lung inflation on f or TE in halothane-anesthetized dogs. Furthermore, hypercapnia increases TI during halothane anesthesia, an effect found after carotid denervation but not found in intact chloralose-urethan-anesthetized dogs. It is suggested that these differences between chloralose-urethan- and halothane-anesthetized dogs may be due to functional carotid chemoreceptor denervation by halothane.

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