Effect of carotid body resection on ventilatory and acid-base control during exercise

1975 ◽  
Vol 39 (3) ◽  
pp. 354-358 ◽  
Author(s):  
K. Wasserman ◽  
B. J. Whipp ◽  
S. N. Koyal ◽  
M. G. Cleary
Keyword(s):  
Steady State ◽  
Metabolic Acidosis ◽  
Carotid Body ◽  
Constant Load ◽  
Incremental Exercise ◽  
Acid Base ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Significant Difference ◽  
Exercise Hyperpnea

To investigate the role of the carotid bodies in exercise hyperpnea and acid-base control, normal and carotid body-resected subjects (CBR) were studied during constant-load and incremental exercise. There was no significant difference in the first-breath ventilatory responses to exercise between the groups; some subjects in each reproducibly exhibited abrupt responses. The subsequent change in Ve toward steady state was slower in the CBR group. The steady-state ventilatory responses were the same in both groups at work rates below the anaerobic threshold (AT). However, above the AT, the hyperpnea was less marked in the CBR group. Ve and acid-base measurements revealed that the CBR group failed to hyperventilate in response to the metabolic acidosis of either constant-load or incremental exercise. We conclude that the carotid bodies 1) are not responsible for the initial exercise hyperpnea, 2) do affect the time course of Ve to its steady state, and 3) are responsible for the respiratory compensation for the metabolic acidosis of exercise.

Effects of altered CSF [H+] on ventilatory responses to exercise in the awake goat

1988 ◽  
Vol 65 (2) ◽  
pp. 921-927 ◽  
Author(s):  
C. A. Smith ◽  
L. C. Jameson ◽  
J. A. Dempsey
Keyword(s):  
Steady State ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Fold Increase ◽  
Co2 Production ◽  
Acid Base ◽  
Ventilatory Responses ◽  
Exercise Hyperpnea ◽  
Acid Base Status ◽  
Response To Exercise

We investigated the effects of selective large changes in the acid-base environment of medullary chemoreceptors on the control of exercise hyperpnea in unanesthetized goats. Four intact and two carotid body-denervated goats underwent cisternal perfusion with mock cerebrospinal fluid (CSF) of markedly varying [HCO-3] (CSF [H+] = 21-95 neq/l; pH 7.68-7.02) until a new steady state of alveolar hypo- or hyperventilation was reached [arterial PCO2 (PaCO2) = 31-54 Torr]. Perfusion continued as the goats completed two levels of steady-state treadmill walking [2 to 4-fold increase in CO2 production (VCO2)]. With normal acid-base status in CSF, goats usually hyperventilated slightly from rest through exercise (-3 Torr PaCO2, rest to VCO2 = 1.1 l/min). Changing CSF perfusate [H+] changed the level of resting PaCO2 (+6 and -4 Torr), but with few exceptions, the regulation of PaCO2 during exercise (delta PaCO2/delta VCO2) remained similar regardless of the new ventilatory steady state imposed by changing CSF [H+]. Thus the gain (slope) of the ventilatory response to exercise (ratio of change in alveolar ventilation to change in VCO2) must have increased approximately 15% with decreased resting PaCO2 (acidic CSF) and decreased approximately 9% with increased resting PaCO2 (alkaline CSF). A similar effect of CSF [H+] on resting PaCO2 and on delta PaCO2/VCO2 during exercise also occurred in two carotid body-denervated goats. Our results show that alteration of the gain of the ventilatory response to exercise occurs on acute alterations in resting PaCO2 set point (via changing CSF [H+]) and that the primary stimuli to exercise hyperpnea can operate independently of central or peripheral chemoreception.

Response time and sensitivity of the ventilatory response to CO2 in unanesthetized intact dogs: central vs. peripheral chemoreceptors

2006 ◽  
Vol 100 (1) ◽  
pp. 13-19 ◽  
Author(s):  
C. A. Smith ◽  
J. R. Rodman ◽  
B. J. A. Chenuel ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Steady State ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Periodic Breathing ◽  
Ventilatory Responses ◽  
Central Chemoreceptors ◽  
Carotid Bodies ◽  
Carotid Body Chemoreceptors ◽  
Relative Gains ◽  
Ventilatory Response To Co2

We assessed the speed of the ventilatory response to square-wave changes in alveolar Pco2 and the relative gains of the steady-state ventilatory response to CO2 of the central chemoreceptors vs. the carotid body chemoreceptors in intact, unanesthetized dogs. We used extracorporeal perfusion of the reversibly isolated carotid sinus to maintain normal tonic activity of the carotid body chemoreceptor while preventing it from sensing systemic changes in CO2, thereby allowing us to determine the response of the central chemoreceptors alone. We found the following. 1) The ventilatory response of the central chemoreceptors alone is 11.2 (SD = 3.6) s slower than when carotid bodies are allowed to sense CO2 changes. 2) On average, the central chemoreceptors contribute ∼63% of the gain to steady-state increases in CO2. There was wide dog-to-dog variability in the relative contributions of central vs. carotid body chemoreceptors; the central exceeded the carotid body gain in four of six dogs, but in two dogs carotid body gain exceeded central CO2 gain. If humans respond similarly to dogs, we propose that the slower response of the central chemoreceptors vs. the carotid chemoreceptors prevents the central chemoreceptors from contributing significantly to ventilatory responses to rapid, transient changes in arterial Pco2 such as those after periods of hypoventilation or hyperventilation (“ventilatory undershoots or overshoots”) observed during sleep-disordered breathing. However, the greater average responsiveness of the central chemoreceptors to brain hypercapnia in the steady-state suggests that these receptors may contribute significantly to ventilatory overshoots once unstable/periodic breathing is fully established.

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.

Role of the carotid bodies in chemosensory ventilatory responses in the anesthetized mouse

2004 ◽  
Vol 97 (4) ◽  
pp. 1401-1407 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Mieczyslaw Pokorski ◽  
Ikuo Homma
Keyword(s):  
Tidal Volume ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Whole Body ◽  
Sudden Increase ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Before And After ◽  
Carotid Body Denervation

We examined the effects of carotid body denervation on ventilatory responses to normoxia (21% O2 in N2 for 240 s), hypoxic hypoxia (10 and 15% O2 in N2 for 90 and 120 s, respectively), and hyperoxic hypercapnia (5% CO2 in O2 for 240 s) in the spontaneously breathing urethane-anesthetized mouse. Respiratory measurements were made with a whole body, single-chamber plethysmograph before and after cutting both carotid sinus nerves. Baseline measurements in air showed that carotid body denervation was accompanied by lower minute ventilation with a reduction in respiratory frequency. On the basis of measurements with an open-circuit system, no significant differences in O2 consumption or CO2 production before and after chemodenervation were found. During both levels of hypoxia, animals with intact sinus nerves had increased respiratory frequency, tidal volume, and minute ventilation; however, after chemodenervation, animals experienced a drop in respiratory frequency and ventilatory depression. Tidal volume responses during 15% hypoxia were similar before and after carotid body denervation; during 10% hypoxia in chemodenervated animals, there was a sudden increase in tidal volume with an increase in the rate of inspiration, suggesting that gasping occurred. During hyperoxic hypercapnia, ventilatory responses were lower with a smaller tidal volume after chemodenervation than before. We conclude that the carotid bodies are essential for maintaining ventilation during eupnea, hypoxia, and hypercapnia in the anesthetized mouse.

Acid-base alterations and plasma potassium concentration

1959 ◽  
Vol 197 (2) ◽  
pp. 319-326 ◽  
Author(s):  
Daniel H. Simmons ◽  
Melvin Avedon
Keyword(s):  
Steady State ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Alveolar Ventilation ◽  
Acid Base ◽  
Blood Ph ◽  
Arterial Ph ◽  
Significant Difference ◽  
Anesthetized Dogs ◽  
K Concentration

Arterial pH of anesthetized dogs was held constant during infusion of HCl or NaHCO3 by appropriate alterations in alveolar ventilation. While plasma potassium concentration dropped somewhat (presumably due to gradual potassium depletion), there was no significant difference in plasma potassium during the two types of infusions. The implication is that metabolic and respiratory acid-base disturbances having comparable effects on pH also have similar effects on the plasma potassium concentration. Other data support this conclusion and also indicate that effects of acidosis and alkalosis are quantitatively similar. On the basis of data of this study and of other data in the literature, it appears that the ratio of change in potassium concentration to change in blood pH ordinarily averages –3.0 to –5.0 in a steady state and that achieving a steady state requires 1–2 hours of equilibration. Data are presented which support the concept that extracellular K concentration, rather than total extracellular K, is physiologically regulated and that this involves rapid exchanges with intracellular K.

Independence of exercise hyperpnea and acidosis during high-intensity exercise in ponies

1986 ◽  
Vol 60 (3) ◽  
pp. 1016-1024 ◽  
Author(s):  
L. G. Pan ◽  
H. V. Forster ◽  
G. E. Bisgard ◽  
C. L. Murphy ◽  
T. F. Lowry
Keyword(s):  
Carotid Body ◽  
High Intensity ◽  
Treadmill Exercise ◽  
Constant Load ◽  
Normal Group ◽  
High Intensity Exercise ◽  
Arterial Pco2 ◽  
Exercise Hyperpnea ◽  
Constant Load Exercise

We investigated arterial PCO2 (PaCO2) and pH (pHa) responses in ponies during 6-min periods of high-intensity treadmill exercise. Seven normal, seven carotid body-denervated (2 wk-4 yr) (CBD), and five chronic (1–2 yr) lung (hilar nerve)-denervated (HND) ponies were studied during three levels of constant load exercise (7 mph-11%, 7 mph-16%, and 7 mph-22% grade). Mean pHa for each group of ponies became alkaline in the first 60 s (between 7.45 and 7.52) (P less than 0.05) at all work loads. At 6 min pHa was at or above rest at 7 mph-11%, moderately acidic at 7 mph-16% (7.32–7.35), and markedly acidic at 7 mph-22% (7.20–7.27) for all groups of ponies. Yet with no arterial acidosis at 7 mph 11%, normal ponies decreased PaCO2 below rest (delta PaCO2) by 5.9 Torr at 90 s and 7.8 Torr by 6 min of exercise (P less than 0.05). With a progressively more acid pHa at the two higher work loads in normal ponies, delta PaCO2 was 7.3 and 7.8 Torr by 90 s and 9.9 and 11.4 Torr by 6 min, respectively (P less than 0.05). CBD ponies became more hypocapnic than the normal group at 90 s (P less than 0.01) and tended to have greater delta PaCO2 at 6 min. The delta PaCO2 responses in normal and HND ponies were not significantly different (P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory responses to intravenous and airway CO2 administration in anesthetized dogs

1980 ◽  
Vol 48 (2) ◽  
pp. 337-346 ◽  
Author(s):  
W. E. Fordyce ◽  
F. S. Grodins
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Loading Rate ◽  
Blood Flow Rate ◽  
Time Dependent ◽  
Base Line ◽  
Ventilatory Responses ◽  
Significant Difference ◽  
Anesthetized Dogs ◽  
Randomized Protocol

The ventilatory responses to steady-state venous CO2 loading (iv CO2) and CO2 inhalation have been observed in chloralose-urethan-anesthetized dogs. Intravenous CO2 was administered by increasing the CO2 fraction of gas ventilating a membrane gas exchanger in an arteriovenous bypass; blood flow rate was fixed at 30 ml/min. During the study, we identified a time-dependent hyperventilation in all 14 experimentally treated dogs and in 4 additional sham-treated dogs. When we tested 8 of these animals with a protocol having small progressive increments in iv CO2 loading rate, we observed a response approaching isocapnia during iv CO2 and a large hypocapnia when we returned to control conditions. The use of a randomized protocol in 6 animals demonstrated the necessity of accounting for this systematic base-line shift, because before doing so the response depended more on the passage of time than on the nature of the CO2 load. After this analytical adjustment was made, there was no significant difference between the respiratory controller gains (delta nu E/delta Paco2) for inhaled and iv CO2.

scholarly journals The analysis of acid-base balance in haemodialyzed patients and the effect of etiology of chronic renal failure on acid-base parameter values

2004 ◽  
Vol 23 (2) ◽  
pp. 175-178
Author(s):  
Emina Colak ◽  
Sanja Stankovic ◽  
Nada Majkic-Singh ◽  
Milan Radovic
Keyword(s):  
Renal Failure ◽  
Metabolic Acidosis ◽  
Chronic Renal Failure ◽  
Underlying Disease ◽  
Tubular Secretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Significant Difference ◽  
Before And After ◽  
Base Balance

Due to reduced scope of renal function in chronic renal failure (CRF) it is not rare that it comes to marked metabolic acidosis and pathologic catabolism associated with hypoxia. The cause of metabolic acidosis is deminished tubular secretion of ammonia, due to reduced synthesis, stipulated by lower number of renal canaliculi. Acid-base balance was analyzed in 74 patients suffering from CRF who were on haemodialysis program. Heparinised blood was taken from these patients before and after haemodialysis in which the following parameters were measured: pH, pCO2, pO2, HCO-3 ?, TCO2. The aim of this study was the monitoring of patients' acid-base status before and after haemodilalysis in order to evaluate the degree of stabilization of acid-base balance after haemodilalysis and also to define the correlation between the etiology of CRF and the degree of acid-base balance disorder. In relation to underlying disease resulting in CRF, the patients were divided into five groups: I-tubular interstitial nephrosis (TIN), II-polycystic kidney disease (ADPKD), III-glomerulonephritis (GN), IVhypertension and nephroangio-sclerosis (HTA-Nascl) and V-consisting of patients whose underlying disease was not diagnosed (ERSD). The obtained values of pH, HCO2 and TCO2 after haemodialysis (pH = 7.428 ? 0.06; HCO-3 ?= 25.4 ? 3.44 mmol/L; TCO2 = 26.57 ? 3.56 mmol/L), were significantly increased (p<0.001), in relation to values before haemodialysis (pH = 7.350 ? 0.05; HCO-3 ?= 20.88 ? 2.92 mmol/L; TCO2 = 22.03 ? 3.00 mmol/L). There was no statistically significant difference in values of measured parameters (p>0.05) in relation to underlying disease either before or after haemodialysis both in males and females.

A Comparison of the Ventilatory Response to Carbon Dioxide by Steady-State and Rebreathing Methods during Metabolic Acidosis and Alkalosis

1973 ◽  
Vol 45 (2) ◽  
pp. 239-249 ◽  
Author(s):  
R. A. F. Linton ◽  
P. A. Poole-Wilson ◽  
R. J. Davies ◽  
I. R. Cameron
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Metabolic Acidosis ◽  
Normal Subjects ◽  
Respiratory Response ◽  
Acid Base ◽  
Co2 Response ◽  
Significant Change ◽  
Response Line ◽  
Rebreathing Methods

1. The rebreathing and steady-state methods for assessing the response to inhaled carbon dioxide were compared in six normal subjects under control conditions and during metabolic acidosis and alkalosis. 2. The slopes of the CO2 response lines obtained with the two methods under control conditions were not significantly different. 3. Metabolic acidosis and alkalosis produced a significant change in the intercept of the response line when this was assessed with the steady-state technique. The slope of the response lines did not change significantly in alkalosis but there was probably a small increase during acidosis. 4. Using the rebreathing technique there was no significant change in intercept in acidosis and alkalosis, but the slope varied significantly from control values. 5. It is concluded that the two methods of assessing the respiratory response to inhaled CO2 are comparable under normal acid-base conditions. This similarity does not hold in metabolic changes of the acid-base state.

Dopamine and ventilatory effects of hypoxia and almitrine in chronically hypoxic rats

1989 ◽  
Vol 67 (1) ◽  
pp. 186-192 ◽  
Author(s):  
R. A. Wach ◽  
D. Bee ◽  
G. R. Barer
Keyword(s):  
Carotid Body ◽  
Ventilatory Response ◽  
Response Curves ◽  
Enhancing Effect ◽  
Stimulus Response ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Ventilatory Effects ◽  
Ventilatory Response To Hypoxia

We hypothesized that the temporary blunted ventilatory response to hypoxia seen in chronically hypoxic rats could be related to the increased amount of dopamine found in their carotid bodies. Rats, kept 2–3 wk in 10% O2, showed reduced nonisocapnic ventilatory responses to 21–12% inspiratory O2 fraction compared with control rats. Stimulus-response curves to almitrine, which simulates the action of hypoxia on the carotid body, were also depressed in chronically hypoxic rats. Responses to hypoxia and almitrine were significantly correlated in the two groups of rats. Dopamine depressed ventilation during normoxia, hypoxia, and almitrine stimulation in both groups, an action abolished by the dopamine-2 antagonist domperidone. Domperidone slightly increased responses to hypoxia and almitrine in control rats but had a greater enhancing effect in chronically hypoxic rats, such that there was no longer a difference between the responses of the two groups.

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