Einflu� des O2-Druckes in der Einatmungsluft auf die Atemt�tigkeit des Menschen, gepr�ft unter Konstanthaltung des alveolaren CO2-Druckes

Hh, Loeschchke; Kh, Gertz

doi:10.1007/bf00361733

Cited by 91 publications

(13 citation statements)

References 25 publications

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“…This may have differentially contributed to shortening breath‐hold duration, depending upon the individual's peripheral chemoreceptor response magnitude to increases in the arterial partial pressure of CO 2 , decreases in arterial partial pressure of O 2 and the synergistic relationship between these two stimuli at the carotid body (e.g. Nielsen & Smith, 1952; Loeschcke & Gertz, ; Lahiri & DeLaney, ; Daristotle et al . ).…”

Section: Discussionmentioning

confidence: 99%

“…Transient or steady‐state arterial hypercapnia and/or hypoxia stimulates the carotid bodies, eliciting a peripheral chemoreflex (Nielsen & Smith, ; Loeschcke & Gertz, ; Lahiri & DeLaney, ; Daristotle et al . ).…”

Section: Introductionmentioning

confidence: 99%

“…Transient or steady-state arterial hypercapnia and/or hypoxia stimulates the carotid bodies, eliciting a peripheral chemoreflex (Nielsen & Smith, 1952;Loeschcke & Gertz, 1958;Lahiri & DeLaney, 1975;Daristotle et al 1987). In addition, accumulation of P CO 2 /[H + ] in brain tissue stimulates central chemoreceptors, eliciting a central chemoreflex (Ainslie & Duffin, 2009;Duffin, 2011;Guyenet et al 2010).…”

Section: Introductionmentioning

confidence: 99%

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Quantifying cerebrovascular reactivity in anterior and posterior cerebral circulations during voluntary breath holding

Bruce

Steinback

Chauhan

et al. 2016

Experimental Physiology

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What is the central question of this study? We developed and validated a 'stimulus index' (SI; ratio of end-tidal partial pressures of CO and O ) method to quantify cerebrovascular reactivity (CVR) in anterior and posterior cerebral circulations during breath holding. We aimed to determine whether the magnitude of CVR is correlated with breath-hold duration. What is the main finding and its importance? Using the SI method and transcranial Doppler ultrasound, we found that the magnitude of CVR of the anterior and posterior cerebral circulations is not positively correlated with physiological or psychological break-point during end-inspiratory breath holding. Our study expands the ability to quantify CVR during breath holding and elucidates factors that affect break-point. The central respiratory chemoreflex contributes to blood gas homeostasis, particularly in response to accumulation of brainstem CO . Cerebrovascular reactivity (CVR) affects chemoreceptor stimulation inversely through CO washout from brainstem tissue. Voluntary breath holding imposes alterations in blood gases, eliciting respiratory chemoreflexes, potentially contributing to breath-hold duration (i.e. break-point). However, the effects of cerebrovascular reactivity on break-point have yet to be determined. We tested the hypothesis that the magnitude of CVR contributes directly to breath-hold duration in 23 healthy human participants. We developed and validated a cerebrovascular stimulus index methodology [SI; ratio of end-tidal partial pressures of CO and O (P ET ,CO2/P ET ,O2)] to quantify CVR by correlating measured and interpolated values of P ET ,CO2 (r = 0.95, P < 0.0001), P ET ,O2 (r = 0.98, P < 0.0001) and SI (r = 0.94, P < 0.0001) during rebreathing. Using transcranial Doppler ultrasound, we then quantified the CVR of the middle (MCAv) and posterior (PCAv) cerebral arteries by plotting cerebral blood velocity against interpolated SI during a maximal end-inspiratory breath hold. The MCAv CVR magnitude was larger than PCAv (P = 0.001; +70%) during breath holding. We then correlated MCAv and PCAv CVR with the physiological (involuntary diaphragmatic contractions) and psychological (end-point) break-point, within individuals. There were significant inverse but modest relationships between both MCAv and PCAv CVR and both physiological and psychological break-points (r < -0.53, P < 0.03). However, these relationships were absent when MCAv and PCAv cerebrovascular conductance reactivity was correlated with both physiological and psychological break-points (r > -0.42; P > 0.06). Although central chemoreceptor activation is likely to be contributing to break-point, our data suggest that CVR-mediated CO washout from central chemoreceptors plays no role in determining break-point, probably because of a reduced arterial-to-tissue CO gradient during breath holding.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Quantifying cerebrovascular reactivity in anterior and posterior cerebral circulations during voluntary breath holding

Bruce

Steinback

Chauhan

et al. 2016

Experimental Physiology

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“…Interestingly, the wasting disorder resembles the effect of chronic neonatal hypoxia and could, in fact, be secondary to a respiratory defect (Mortola, 2001). Finally, differences in metabolic rate are unlikely to explain the differential effects of genotype on the overall ventilatory response to CO 2 , as the ventilatory response to CO 2 is linear throughout most of the physiological range (Loeschke & Gertz, 1958).…”

Section: Discussionmentioning

confidence: 99%

Sudden neonatal death in PACAP‐deficient mice is associated with reduced respiratory chemoresponse and susceptibility to apnoea

Cummings

Pendlebury

Sherwood

et al. 2004

The Journal of Physiology

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Pituitary adenylate cyclase-activating polypeptide (PACAP)-deficient mice are more prone to sudden death during postnatal weeks 1-3 than wild-type littermates. Given that PACAP is localized in brainstem regions associated with respiratory chemosensitivity, we examined whether PACAP-null neonates have reduced respiratory responses to hypoxia and hypercapnia. Using unrestrained, whole-body, flow-through plethysmography we found that, by postnatal day 4, the PACAP-null neonates had significantly reduced ventilation during baseline breathing, and blunted responses to both hypoxia (10% O 2 -90% N 2 ) and hypercapnia (8% CO 2 -92% air). To determine whether the respiratory phenotype of the PACAP-null mice may contribute to their greater neonatal mortality, we used ECG to examine respiration and cardiovascular function of littermates. We demonstrate that, under conditions that exacerbate mortality of knockout but not wild-type animals, PACAP-deficient mice experience prolonged apnoeas that precede atrioventricular block. Both apnoeas and atrio-ventricular block were absent in wild-type littermates. These data suggest that PACAP-deficiency results in higher neonatal mortality primarily as a result of respiratory control defects and raise the possibility that mutations in genes encoding components of the PACAP signalling pathways may contribute to neonatal breathing disorders in humans.

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“…The use of progressive hypoxia at constant Pco2 as a technique for determining the ventilatory response to hypoxia was described by Loeschcke and Gertz (18).…”

Section: Methodsmentioning

confidence: 99%

Attenuation of the Ventilatory and Heart Rate Responses to Hypoxia and Hypercapnia with Aging in Normal Men

Kronenberg¹,

Drage²

1973

J. Clin. Invest.

355

134

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A B S T R A C T The response of ventilation and of heart rate to hypoxia and hypercapnia was determined in eight young normal men age 22-30 yr and eight elderly men age 64-73. The elderly men were selected and carefully screened to eliminate the possibility of cardiopulmonary disease. All the subjects were born at low altitude and had no significant prior exposure to hypoxia. The ventilatory response to hypoxia was measured as the exponential slope constant, k, of regression lines relating the logarithm of incremental ventilation to PAo, during isocapnic progressive hypoxia. The heart rate response to hypoxia was measured as the percentage change in heart rate between PAO2 = 100 and PAO2 = 40 mm Hg. The ventilatory response to hypercapnia was measured as the slope of regression lines relating ventilation to PACO2 during rebreathing with PAO2> 200 mm Hg. The heart rate response to hypercapnia was measured as the percentage change in heart rate between control values at the start of the rebreathing test and PACO2= 55 mm Hg.The ventilatory and heart rate responses to both hypoxia and hypercapnia were significantly decreased in the elderly men as compared to the young men. Hypoxic ventilatory drive was decreased by 51±6% (mean +-SEM; P < 0.001) and hypercapnic drive by 41±7% (P < 0.025). The percentage change in heart rate produced by hypoxia was 34±5% (mean +SEM) in the young normals and 12±2% in the old normals (P < 0.005). Similar figures for heart rate in response to hypercapnia were 15±3% and -1±1% for the young and old normal groups (P < 0.001).We conclude that ventilatory and heart rate responses to hypoxia and hypercapnia diminish with age. These alterations in both ventilatory and circulatory controls could make older individuals more vulnerable to hypoxic disease states.

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Einflu� des O2-Druckes in der Einatmungsluft auf die Atemt�tigkeit des Menschen, gepr�ft unter Konstanthaltung des alveolaren CO2-Druckes

Cited by 91 publications

References 25 publications

Quantifying cerebrovascular reactivity in anterior and posterior cerebral circulations during voluntary breath holding

Quantifying cerebrovascular reactivity in anterior and posterior cerebral circulations during voluntary breath holding

Sudden neonatal death in PACAP‐deficient mice is associated with reduced respiratory chemoresponse and susceptibility to apnoea

Attenuation of the Ventilatory and Heart Rate Responses to Hypoxia and Hypercapnia with Aging in Normal Men

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