Central-peripheral chemoreceptor interaction in awake cerebrospinal fluid-perfused goats

1984 ◽  
Vol 56 (6) ◽  
pp. 1541-1549 ◽  
Author(s):  
C. A. Smith ◽  
L. C. Jameson ◽  
G. S. Mitchell ◽  
T. I. Musch ◽  
J. A. Dempsey
Keyword(s):  
Tidal Volume ◽  
Dose Response ◽  
Minute Ventilation ◽  
Extracellular Fluid ◽  
Breathing Frequency ◽  
Response Curves ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Responses ◽  
Average Slope ◽  
Response Line

We assessed the ventilatory interaction between central [central nervous system (CNS)] and peripheral chemoreceptor stimuli in five awake goats. CNS extracellular fluid (ECF) [H+] was altered with cisterna magna perfusion of mock CSF. Peripheral chemoreceptors were stimulated with three doses of NaCN given intravenously. The resulting dose-response curves were used to assess interaction of the central and peripheral stimuli. The observed interaction was hypoadditive; i.e., the average slope of the NaCN-inspired minute ventilation dose-response line was significantly greater during alkaline perfusion than during acidic perfusion. This correlation can be described by slope = -0.24 (CSF [H+]) + 30.7; r = 0.67 (P less than 0.01). Increased ventilatory responses were accompanied by increases in mean inspiratory flow, tidal volume, and breathing frequency and decreases in expiratory time in response to peripheral chemoreceptor stimulation. Unlike previous reports in anesthetized and denervated animals, in our awake intact goats the ventilatory and tidal volume responses showed no significant dependence on the level of control (pre-NaCN stimulus) inspired minute ventilation. We conclude that the level of [H+] in cerebral ECF exerts a significant reflex-mediated hypoadditive effect on the ventilatory responses to peripheral chemoreceptor stimulation.

Adaptations of quadriplegic men to consecutively loaded breaths

1984 ◽  
Vol 56 (4) ◽  
pp. 1099-1103 ◽  
Author(s):  
K. Axen
Keyword(s):  
Tidal Volume ◽  
Sensory Input ◽  
Minute Ventilation ◽  
Breathing Frequency ◽  
Ventilatory Responses ◽  
Group Response ◽  
Resistive Loading ◽  
Elastic Loading ◽  
Resistive Loads ◽  
Accessory Muscles

Ventilatory responses to graded elastic and resistive loads from 20 quadriplegic men were analyzed. During the 1st, 5th, and 10th consecutively loaded inspirations 1) responses from different subjects ranged from a weak tidal volume defense coupled with an increased breathing frequency to a strong tidal volume defense coupled with a decreased frequency; 2) strong tidal volume defenders generally employed longer inspirations than did weak tidal volume defenders; and 3) individual respiratory frequencies were mediated by similar changes in inspiratory and/or expiratory timing. Thus the group response was qualitatively similar on the 1st, 5th, and 10th loaded breaths. Quantitatively, however, minute ventilation increased throughout each 10-breath episode due to progressively larger tidal volumes coupled with equal breathing frequencies. These larger tidal volumes were due to progressively stronger inspirations with no changes in timing during elastic loading, whereas they were due to both stronger and longer inspirations during resistive loading. These findings, which are qualitatively the same as those found in healthy subjects, indicate that sensory input from the mouth, lung, and diaphragm, and motor output to the diaphragm and accessory muscles are sufficient, by themselves, to mediate normal patterns of ventilatory adjustments during consecutively loaded breaths.

Peripheral chemoreceptor function in children with the congenital central hypoventilation syndrome

1993 ◽  
Vol 74 (1) ◽  
pp. 379-387 ◽  
Author(s):  
D. Gozal ◽  
C. L. Marcus ◽  
D. Shoseyov ◽  
T. G. Keens
Keyword(s):  
Vital Capacity ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Clinical Manifestations ◽  
Congenital Central Hypoventilation Syndrome ◽  
Tidal Breathing ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Responses ◽  
Central Hypoventilation ◽  
Hypoventilation Syndrome

In children with the congenital central hypoventilation syndrome (CCHS), some patients require mechanical ventilation during sleep, whereas others need respiratory assistance even when awake. The cause of this disparity is unclear. We hypothesized that differences in peripheral chemoreceptor response (PCR) could provide an explanatory mechanism for this disparity in clinical manifestations. PCR was measured in five children with CCHS and five sex- and age-matched controls by measuring the ventilatory responses induced by 100% O2 breathing, five tidal breaths of 100% N2, and vital capacity breaths of 5% and 15% CO2 in O2 and 5% CO2–95% N2. Tidal breathing of 100% O2 resulted in similar ventilatory responses in CCHS patients and controls with various changes dependent on the method of analysis of response used. Acute hypoxia by N2 tidal breathing resulted in a 39.2 +/- 22% increase in respiratory rate in CCHS patients and a 15.1 +/- 11.1% increase in controls (P < 0.05), with similar increases in minute ventilation (VE) of 124 +/- 69% and 85 +/- 11%, respectively. Vital capacity breaths of each of the CO2-containing gas mixtures induced similar increases in VE in CCHS patients and controls. The changes in VE obtained with 15% CO2–85% O2 and with 5% CO2–95% N2 were significantly greater than those with 5% CO2–95% O2, suggesting a dose-dependent response as well as additive effects of hypercapnic and hypoxic stimuli. We conclude that the PCR, when assessed by acute hypoxia, hyperoxia, or hypercapnia, is present and intact in CCHS children who are able to sustain adequate ventilation during wakefulness.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory and abdominal muscle responses to expiratory threshold loading in cystic fibrosis

1992 ◽  
Vol 72 (3) ◽  
pp. 842-850 ◽  
Author(s):  
F. Cerny ◽  
L. Armitage ◽  
J. A. Hirsch ◽  
B. Bishop
Keyword(s):  
Cystic Fibrosis ◽  
Tidal Volume ◽  
Body Position ◽  
Minute Ventilation ◽  
Abdominal Muscle ◽  
Abdominal Muscles ◽  
Breathing Frequency ◽  
Control Subjects ◽  
Lung Dysfunction ◽  
Muscle Responses

We hypothesized that the hyperinflation and pulmonary dysfunction of cystic fibrosis (CF) would distort feedback and therefore alter the abdominal muscle response to graded expiratory threshold loads (ETLs). We compared the respiratory and abdominal muscle responses with graded ETLs of seven CF patients with severe lung dysfunction with those of matched healthy control subjects in the supine and 60 degrees head-up positions. Breathing frequency, tidal volume, and ventilatory timing were determined from inspiratory flow recordings. Abdominal electromyograms (EMGs) were detected with surface electrodes placed unilaterally over the external and internal oblique and the rectus abdominis muscles. Thresholds, times of onset, and durations of phasic abdominal activity were determined from raw EMGs; peak amplitudes were determined from integrated EMGs. Graded ETLs were imposed by submerging a tube from the expiratory port of the breathing valve into a column of water at depths of 0–25 cmH2O. We found that breathing frequency, tidal volume, and expired minute ventilation were higher in CF patients than in control subjects during low ETLs; a change in body position did not alter these ventilatory responses in the CF patients but did in the control subjects. All CF patients, but none of the control subjects, had tonic abdominal activity while supine. CF patients recruited abdominal muscles at lower loads, earlier in the respiratory cycle, and to a higher recruitment level in both positions than the control subjects, but burst duration of phasic activity was not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of acute and chronic acetazolamide on resting ventilation and ventilatory responses in men

1993 ◽  
Vol 74 (1) ◽  
pp. 230-237 ◽  
Author(s):  
E. R. Swenson ◽  
J. M. Hughes
Keyword(s):  
Metabolic Acidosis ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Acidosis ◽  
Acute Effects ◽  
Acid Base Balance ◽  
Ventilatory Control ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Responses ◽  
Base Balance

The effects of acetazolamide (ACTZ) on ventilatory control are thought to be mediated by metabolic acidosis. However, carbonic anhydrase (CA) inhibition within brain and chemoreceptors and tissue respiratory acidosis may also be important. We compared the acute effects of ACTZ (tissue respiratory acidosis and tissue CA inhibition without metabolic acidosis) on ventilation and ventilatory control with chronic ACTZ (acute effects plus metabolic acidosis). Five men were studied 1 h after 500 mg iv ACTZ or 0.9% saline (acute effects) and also after three doses of ACTZ (500 mg po every 6 h; chronic effects). Minute ventilation (VE), steady-state hypercapnic ventilatory response (HCVR), and hypoxic ventilatory response (HVR) were measured with respiratory inductance plethysmography. Resting VE was increased equally by acute and chronic ACTZ. HCVR increased with chronic ACTZ in hyperoxia and even further in hypoxia. In contrast, acute ACTZ had no effect on the HCVR slope in hyperoxia and suppressed its augmentation by hypoxia. HVR was fully suppressed by acute ACTZ but unchanged with chronic ACTZ. ACTZ also slowed the rate of full ventilatory response to CO2. These findings show that CA inhibitors affect ventilatory control in a complex fashion, not only through changes in systemic acid-base balance but also by central and peripheral chemoreceptor inhibition.

Effect of acute hypoxia on respiration and brain stem blood flow in the piglet

1991 ◽  
Vol 70 (1) ◽  
pp. 251-259 ◽  
Author(s):  
R. A. Darnall ◽  
G. Green ◽  
L. Pinto ◽  
N. Hart
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Extracellular Fluid ◽  
Respiratory Drive ◽  
Peripheral Chemoreceptor ◽  
Before And After ◽  
Spontaneously Breathing ◽  
Local Brain

Changes in local brain stem perfusion that alter extracellular fluid Pco2 and/or [H+] near central chemoreceptors may contribute to the decrease in respiration observed during hypoxia after peripheral chemoreceptor denervation and to the delayed decrease observed during hypoxia in the newborn. In this study, we measured the changes in respiration and brain stem blood flow (BBF) during 2–4 min of hypoxic hypoxia in both intact and denervated piglets and calculated the changes in brain stem Pco2 and [H+] that would be expected to occur as a result of the changes in BBF. All animals were anesthetized, spontaneously breathing, and between 2 and 7 days of age. Respiratory and other variables were measured before and during hypoxia in all animals, and BBF (microspheres) was measured in a subgroup of intact and denervated animals at 0, 30, and 260 s and at 0 and 80 s, respectively. During hypoxia, minute ventilation increased and then decreased (biphasic response) in the intact animals but decreased only in the denervated animals. BBF increased in a near linear fashion, and calculated brain stem extracellular fluid Pco2 and [H+] decreased over the first 80 s both before and after denervation. We speculate that a rapid increase in BBF during acute hypoxia decreases brain stem extracellular fluid Pco2 and [H+], which, in turn, negatively modulate the increase in respiratory drive produced by peripheral chemoreceptor input to the central respiratory generator.

Tachykinins mediate bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs

1989 ◽  
Vol 66 (3) ◽  
pp. 1108-1112 ◽  
Author(s):  
D. W. Ray ◽  
C. Hernandez ◽  
A. R. Leff ◽  
J. M. Drazen ◽  
J. Solway
Keyword(s):  
Tidal Volume ◽  
Guinea Pigs ◽  
Minute Ventilation ◽  
Response Curves ◽  
Mechanically Ventilated ◽  
Stimulus Response ◽  
Respiratory System Resistance ◽  
Water Saturated ◽  
And Control ◽  
Isocapnic Hyperpnea

We tested the hypothesis that tachykinins mediate hyperpnea-induced bronchoconstriction (HIB) in 28 guinea pigs. Stimulus-response curves to increasing minute ventilation with dry gas were generated in animals depleted of tachykinins by capsaicin pretreatment and in animals pretreated with phosphoramidon, a neutral metalloendopeptidase inhibitor. Sixteen anesthetized guinea pigs received capsaicin (50 mg/kg sc) after aminophylline (10 mg/kg ip) and terbutaline (0.1 mg/kg sc). An additional 12 animals received saline (1 ml sc) instead of capsaicin. One week later, all animals were anesthetized, given propranolol (1 mg/kg iv), and mechanically ventilated (6 ml/kg, 60 breaths/min, 50% O2 in air fully water saturated). Phosphoramidon (0.5 mg iv) was administered to five of the noncapsaicin-treated guinea pigs. Eucapnic dry gas (95% O2–5% CO2) hyperpnea “challenges” were performed by increasing the tidal volume (2–6 ml) and frequency (150 breaths/min) for 5 min. Capsaicin-pretreated animals showed marked attenuation in HIB, with a rightward shift of the stimulus-response curve compared with controls; the estimated tidal volume required to elicit a twofold increase in respiratory system resistance (ES200) was 5.0 ml for capsaicin-pretreated animals vs. 3.7 ml for controls (P less than 0.03). Phosphoramidon-treated animals were more reactive to dry gas hyperpnea compared with control (ES200 = 2.6 ml; P less than 0.0001). Methacholine dose-response curves (10(-11) to 10(-7) mol iv) obtained at the conclusion of the experiments were similar among capsaicin, phosphoramidon, and control groups. These findings implicate tachykinin release as an important mechanism of HIB in guinea pigs.

scholarly journals Ventilatory responses during and following hypercapnic gas challenge are impaired in male but not female endothelial NOS knock-out mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paulina M. Getsy ◽  
Sripriya Sundararajan ◽  
Walter J. May ◽  
Graham C. von Schill ◽  
Dylan K. McLaughlin ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Whole Body ◽  
Inspiratory Time ◽  
Male And Female ◽  
Knock Out ◽  
Ventilatory Responses ◽  
Knock Out Mice ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

AbstractThe roles of endothelial nitric oxide synthase (eNOS) in the ventilatory responses during and after a hypercapnic gas challenge (HCC, 5% CO2, 21% O2, 74% N2) were assessed in freely-moving female and male wild-type (WT) C57BL6 mice and eNOS knock-out (eNOS-/-) mice of C57BL6 background using whole body plethysmography. HCC elicited an array of ventilatory responses that were similar in male and female WT mice, such as increases in breathing frequency (with falls in inspiratory and expiratory times), and increases in tidal volume, minute ventilation, peak inspiratory and expiratory flows, and inspiratory and expiratory drives. eNOS-/- male mice had smaller increases in minute ventilation, peak inspiratory flow and inspiratory drive, and smaller decreases in inspiratory time than WT males. Ventilatory responses in female eNOS-/- mice were similar to those in female WT mice. The ventilatory excitatory phase upon return to room-air was similar in both male and female WT mice. However, the post-HCC increases in frequency of breathing (with decreases in inspiratory times), and increases in tidal volume, minute ventilation, inspiratory drive (i.e., tidal volume/inspiratory time) and expiratory drive (i.e., tidal volume/expiratory time), and peak inspiratory and expiratory flows in male eNOS-/- mice were smaller than in male WT mice. In contrast, the post-HCC responses in female eNOS-/- mice were equal to those of the female WT mice. These findings provide the first evidence that the loss of eNOS affects the ventilatory responses during and after HCC in male C57BL6 mice, whereas female C57BL6 mice can compensate for the loss of eNOS, at least in respect to triggering ventilatory responses to HCC.

Ventilation

2021 ◽  
pp. 56-62
Author(s):  
William J.M. Kinnear ◽  
James H. Hull
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Forced Expiratory Volume ◽  
Peak Exercise ◽  
Breathing Frequency ◽  
Dysfunctional Breathing

This chapter describes how the amount of air going in and out of the lungs increases on exercise. The predicted value for minute ventilation (VE) is calculated for each subject from their own forced expiratory volume in one second (FEV1), rather than taken from published tables. Normally, ventilation does not limit exercise and VE does not reach 80% of the predicted value. If VE at peak exercise is more than 80% of predicted, it is likely there is something wrong with the lungs. VE increases by a combination of a larger tidal volume and an increase in breathing frequency. The pattern of increase is normally gradual. An erratic pattern suggests dysfunctional breathing.

Effects of voluntary constraining of thoracic displacement during hypercapnia

1987 ◽  
Vol 63 (5) ◽  
pp. 1822-1828 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
N. S. Cherniack ◽  
M. D. Altose
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Free Breathing ◽  
Normal Subjects ◽  
Absolute Difference ◽  
Base Line ◽  
Breathing Frequency ◽  
Inhibitory Feedback ◽  
Function Relationship ◽  
Line Level

The study evaluated the interrelationships between the extent of thoracic movements and respiratory chemical drive in shaping the intensity of the sensation of dyspnea. Normal subjects rated their sensations of dyspnea as PCO2 increased during free rebreathing and during rebreathing while ventilation was voluntarily maintained at a constant base-line level. Another trial evaluated the effects on the intensity of dyspnea, of voluntary reduction in the level of ventilation while PCO2 was held constant. During rebreathing, there was a power function relationship between changes in PCO2 and the intensity of dyspnea. At a given PCO2, constraining tidal volume and breathing frequency to the prerebreathing base-line level resulted in an increase in dyspnea. The fractional differences in the intensity of dyspnea between free and constrained rebreathing were independent of PCO2. However, the absolute difference in the intensity of dyspnea between free and constrained rebreathing enlarged with increasing hypercapnia. At PCO2 of 50 Torr, this difference correlated significantly with the increase in both minute ventilation (r = 0.675) and tidal volume (r = 0.757) above the base line during free rebreathing. Similarly, during steady-state hypercapnia at 50 Torr PCO2, the intensity of dyspnea increased progressively as ventilation was voluntarily reduced from the spontaneously adopted free-breathing level. These results indicate that dyspnea increases with the level of respiratory chemical drive but that the intensity of the sensation is further accentuated when ventilation is constrained below that demanded by the level of chemical drive. This may be explained by a loss of inhibitory feedback from lung or chest wall mechanoreceptors acting on brain stem and/or cortical centers.

Effects of pursed-lips breathing and expiratory resistive loading in healthy subjects

1996 ◽  
Vol 80 (5) ◽  
pp. 1772-1784 ◽  
Author(s):  
J. A. Spahija ◽  
A. Grassino
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
Healthy Subjects ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Abdominal Muscle ◽  
Breathing Frequency ◽  
Muscle Recruitment ◽  
Rib Cage ◽  
Resistive Loading

To examine the effect of pursed-lips breathing (PLB) on breathing pattern and respiratory mechanics, we studied 11 healthy subjects breathing with and without PLB at rest and during steady-state bicycle exercise. Six of these subjects took part in a second study, which compared the effects of PLB to expiratory resistive loading (ERL). PLB was found to prolong expiratory and total breath durations and to promote a slower and deeper breathing pattern. During exercise, the compensatory increase that occurred in tidal volume was not sufficient to counter the reduction in breathing frequency, causing minute ventilation to be reduced. Although ERL similarly caused minute ventilation and breathing frequency to be decreased, unlike PLB, it produced no change in tidal volume and prolonged expiratory and total breath durations to a lesser extent. PLB and ERL increased the expiratory resistance to a comparable degree, also increasing the expiratory resistive work of breathing and promoting greater expiratory rib cage and abdominal muscle recruitment in response to the expiratory loads. End-expiratory lung volume, which was determined from inspiratory capacity maneuvers, was not altered by PLB; however, with ERL it was increased by 0.20 and 0.24 liter during rest and exercise, respectively. Inspiratory muscle recruitment patterns were not altered by PLB at rest, although small increases in the relative contribution of the rib cage/accessory muscles in conjunction with abdominal muscle relaxation occurred during exercise. Similar trends were observed with ERL. We conclude that, although ERL and PLB induce comparable respiratory muscle recruitment responses, they are not equivalent with respect to breathing pattern changes and effect on end-expiratory lung volume.

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