Comparing and characterizing transient and steady‐state tests of the peripheral chemoreflex in humans

Pfoh, Jamie R.; Tymko, Michael M.; Abrosimova, Maria; Boulet, Lindsey M.; Foster, Glen E.; Bain, Anthony R.; Ainslie, Philip N.; Steinback, Craig D.; Bruce, Christina D.; Day, Trevor A.

doi:10.1113/ep085498

Cited by 33 publications

(89 citation statements)

References 57 publications

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“…As discussed by Pfoh et al. (), despite the poikilocapnic nature of the transient hypoxia test, any confounders resulting from fluctuations in end‐tidal CO 2 are avoided when considering transient peak responses. This may apply to ∼70% of our subjects (12 out of 17), in whom desirable reductions in

S_{normalp O_{2}}

were achieved with four or fewer breaths of N 2 .…”

Section: Discussionmentioning

confidence: 99%

Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

Paleczny

Seredyński

Tubek

et al. 2019

Experimental Physiology

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New Findings What is the central question of this research?Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance?Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases. Abstract Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen‐breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real‐time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen‐breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp‐VI; in liters per minute per percentage of blood oxygen saturation (SnormalpO2)], tidal volume [Hyp‐VT; in litres per SnormalpO2], heart rate [Hyp‐HR; in beats per minute per SnormalpO2], systolic [Hyp‐SBP; in millimetres of mercury per SnormalpO2] and mean blood pressure [Hyp‐MAP; in millimetres of mercury per SnormalpO2] and systemic vascular resistance [Hyp‐SVR; in dynes seconds (centimetres)−5 per SnormalpO2] was calculated as the slope of the regression line relating the variable to SnormalpO2, including pre‐ and post‐hypoxic values. The Hyp‐VI and Hyp‐VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp‐VI, −0.30 ± 0.15 versus −0.11 ± 0.09; Hyp‐VT, −0.030 ± 0.024 versus −0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp‐HR, −0.62 ± 0.24 versus −0.71 ± 0.33; Hyp‐MAP, −0.43 ± 0.19 versus −0.47 ± 0.21; Hyp‐SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp‐HR was correlated with Hyp‐SVR (r = −074 and −0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = −0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.

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S_{normalp O_{2}}

were achieved with four or fewer breaths of N 2 .…”

Section: Discussionmentioning

confidence: 99%

Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

Paleczny

Seredyński

Tubek

et al. 2019

Experimental Physiology

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“…5 of Pfoh et al . ). Using

S_{normalc O_{2}}

, our TT‐N 2 test had a much lower HVR than the SS‐ISO test but similar magnitude to that of the SS‐POI test (Fig.…”

mentioning

confidence: 97%

“…5 of Pfoh et al . ). We feel that

S_{normalc O_{2}}

is a more appropriate index for these tests, in part for the following reasons: (i) there is a temporal delay of the peripheral pulse oximeter (e.g.…”

mentioning

confidence: 97%

“…6 B of Pfoh et al . ). Conversely, we found that the magnitude of the TT‐N 2 test (

S_{normalc O_{2}}

) was was much smaller than that of the SS‐ISO (

S_{normalc O_{2}}

; Fig.…”

mentioning

confidence: 97%

“…1 A of Pfoh et al . ); (ii) use

S_{normala O_{2}}

(invasive; expensive; accurate; no temporal resolution); or (iii) use

S_{normalc O_{2}}

(instantaneous calculation from end‐tidal

P_{{normalO}_{2}}

stimulus breath using Severinghaus transform). As we have shown in our study that

S_{normalp O_{2}}

and

S_{normalc O_{2}}

are different during dynamic changes in O 2 , our data serve as a caution to those making HVR measurements, because the calculated HVR magnitude (Δlitres per minute per Δ%) is different between

S_{normalp O_{2}}

and

S_{normalc O_{2}}

.…”

mentioning

confidence: 99%

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Considerations for the use of transient tests of the peripheral chemoreflex in humans: the utility is in the question and the context

Pfoh

Day

2016

Experimental Physiology

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Investigations of hypoxia‐induced deoxyhemoglobin as a contrast agent for cerebral perfusion imaging

Sayin

Schulman

Poublanc

et al. 2022

Human Brain Mapping

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The assessment of resting perfusion measures (mean transit time, cerebral blood flow, and cerebral blood volume) with magnetic resonance imaging currently requires the presence of a susceptibility contrast agent such as gadolinium. Here, we present an initial comparison between perfusion measures obtained using hypoxia‐induced deoxyhemoglobin and gadolinium in healthy study participants. We hypothesize that resting cerebral perfusion measures obtained using precise changes of deoxyhemoglobin concentration will generate images comparable to those obtained using a clinical standard, gadolinium. Eight healthy study participants were recruited (6F; age 23–60). The study was performed using a 3‐Tesla scanner with an eight‐channel head coil. The experimental protocol consisted of a high‐resolution T1‐weighted scan followed by two BOLD sequence scans in which each participant underwent a controlled bolus of transient pulmonary hypoxia, and subsequently received an intravenous bolus of gadolinium. The resting perfusion measures calculated using hypoxia‐induced deoxyhemoglobin and gadolinium yielded maps that looked spatially comparable. There was no statistical difference between methods in the average voxel‐wise measures of mean transit time, relative cerebral blood flow and relative cerebral blood volume, in the gray matter or white matter within each participant. We conclude that perfusion measures generated with hypoxia‐induced deoxyhemoglobin are spatially and quantitatively comparable to those generated from a gadolinium injection in the same healthy participant.

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Comparing and characterizing transient and steady‐state tests of the peripheral chemoreflex in humans

Abstract: New FindingsGiven that the transient tests exploit the temporal domain of the peripheral chemoreceptors and have minimal cardiovascular and cerebrovascular confounders, we suggest that they may have broader utility than previously appreciated.

Cited by 33 publications

References 57 publications

Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

Considerations for the use of transient tests of the peripheral chemoreflex in humans: the utility is in the question and the context

Investigations of hypoxia‐induced deoxyhemoglobin as a contrast agent for cerebral perfusion imaging

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