scholarly journals Methodological and physiological variability within the ventilatory response to hypoxia in humans

2000 ◽  
Vol 88 (5) ◽  
pp. 1924-1932 ◽  
Author(s):  
Shu Zhang ◽  
Peter A. Robbins

Measurement of the acute hypoxic ventilatory response (AHVR) requires careful choice of the hypoxic stimulus. If the stimulus is too brief, the response may be incomplete; if the stimulus is too long, hypoxic ventilatory depression may ensue. The purpose of this study was to compare three different techniques for assessing AHVR, using different hypoxic stimuli, and also to examine the between-day variability in AHVR. Ten subjects were studied, each on six different occasions, which were ≥1 wk apart. On each occasion, AHVR was assessed using three different protocols: 1) protocol SW, which uses square waves of hypoxia; 2) protocol IS, which uses incremental steps of hypoxia; and 3) protocol RB, which simulates an isocapnic rebreathing test. Mean values for hypoxic sensitivity were 1.02 ± 0.48, 1.15 ± 0.55, and 0.93 ± 0.60 (SD) l ⋅ min− 1 ⋅ %− 1for protocols SW, IS, and RB, respectively. These differed significantly ( P < 0.01). The coefficients of variation for measurement of AHVR were 20, 23, and 36% for the three protocols, respectively. These were not significantly different. There was a significant physiological variation in AHVR ( F 50,100 = 3.9, P < 0.001), with a coefficient of variation of 26%. We conclude that there was relatively little systematic variation between the three protocols but that AHVR varies physiologically over time.

1988 ◽  
Vol 65 (3) ◽  
pp. 1050-1054 ◽  
Author(s):  
R. B. Filuk ◽  
D. J. Berezanski ◽  
N. R. Anthonisen

In nine normal subjects we measured the ventilatory response to isocapnic hypoxia with and without an intravenous infusion of 1 mg of somatostatin. Arterial O2 saturation was rapidly lowered to 80 +/- 2% in 2 min and maintained for 30 min. During control experiments, ventilation increased immediately (3-5 min) and then declined so that at 25 min of hypoxia ventilation was little above that in room air. Somatostatin was associated with a small decrease in ventilation while the subjects breathed room air. With hypoxia there was no immediate increase in ventilation for the group as a whole, although an increase was observed in one subject. With somatostatin, after 25 min of hypoxia, mean ventilation was lower than at any other time in the study; as hypoxia was discontinued ventilation increased slightly. Somatostatin causes profound depression of the ventilatory response to hypoxia by a mechanism that is not known but may be central. With somatostatin hypoxia of 25-min duration tends to depress ventilation.


2017 ◽  
Vol 95 (6) ◽  
pp. 681-685 ◽  
Author(s):  
Nina P. Aleksandrova ◽  
Galina A. Danilova ◽  
Viacheslav G. Aleksandrov

We investigated the effect of the major inflammatory cytokine interleukin-1beta (IL-1β) on the ventilatory response to hypoxia. The goal was to test the hypothesis that IL-1β impairs the hypoxic ventilatory response in vivo by indirectly inhibiting respiratory neurons in the brainstem via prostaglandins. Thus, IL-1β was delivered by cerebroventricular injection, and the ventilatory hypoxic response was assessed in anesthetized, spontaneously breathing rats pretreated with or without diclofenac, a nonspecific inhibitor of prostaglandin synthesis. We found that the slope of the ventilatory response to hypoxia decreased almost 2-fold from 10.4 ± 3.02 to 4.06 ± 0.86 mL·min−1·(mm Hg)−1 (–61%) 90 min after administration of IL-1β (p < 0.05). The slope of tidal volume and mean inspiratory flow also decreased from 0.074 ± 0.02 to 0.039 ± 0.01 mL·(mm Hg)−1 (–45%, p < 0.05), and from 0.36 ± 0.07 to 0.2 ± 0.04 mL·s−1·(mm Hg)−1 (–46%, p < 0.05), respectively. Pretreatment with diclofenac blocked these effects. Thus, the data indicate that IL-1β degrades the ventilatory hypoxic response by stimulating production of prostaglandin. The increase of cerebral levels of IL-1β, which is induced by the activation of immune cells in the brain, may impair respiratory chemoreflexes.


1989 ◽  
Vol 67 (2) ◽  
pp. 797-803 ◽  
Author(s):  
B. Hannhart ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
L. G. Moore

Pregnancy increases ventilation and ventilatory sensitivity to hypoxia and hypercapnia. To determine the role of the carotid body in the increased hypoxic ventilatory response, we measured ventilation and carotid body neural output (CBNO) during progressive isocapnic hypoxia in 15 anesthetized near-term pregnant cats and 15 nonpregnant females. The pregnant compared with nonpregnant cats had greater room-air ventilation [1.48 +/- 0.24 vs. 0.45 +/- 0.05 (SE) l/min BTPS, P less than 0.01], O2 consumption (29 +/- 2 vs. 19 +/- 1 ml/min STPD, P less than 0.01), and lower end-tidal PCO2 (30 +/- 1 vs. 35 +/- 1 Torr, P less than 0.01). Lower end-tidal CO2 tensions were also observed in seven awake pregnant compared with seven awake nonpregnant cats (28 +/- 1 vs. 31 +/- 1 Torr, P less than 0.05). The ventilatory response to hypoxia as measured by the shape of parameter A was twofold greater (38 +/- 5 vs. 17 +/- 3, P less than 0.01) in the anesthetized pregnant compared with nonpregnant cats, and the CBNO response to hypoxia was also increased twofold (58 +/- 11 vs. 29 +/- 5, P less than 0.05). The increased CBNO response to hypoxia in the pregnant compared with the nonpregnant cats persisted after cutting the carotid sinus nerve while recording from the distal end, indicating that the increased hypoxic sensitivity was not due to descending central neural influences. We concluded that greater carotid body sensitivity to hypoxia contributed to the increased hypoxic ventilatory responsiveness observed in pregnant cats.


1987 ◽  
Vol 63 (5) ◽  
pp. 1884-1889 ◽  
Author(s):  
M. Vizek ◽  
C. K. Pickett ◽  
J. V. Weil

There is considerable interindividual variation in ventilatory response to hypoxia in humans but the mechanism remains unknown. To examine the potential contribution of variable peripheral chemorecptor function to variation in hypoxic ventilatory response (HVR), we compared the peripheral chemoreceptor and ventilatory response to hypoxia in 51 anesthetized cats. We found large interindividual differences in HVR spanning a sevenfold range. In 23 cats studied on two separate days, ventilatory measurements were correlated (r = 0.54, P less than 0.01), suggesting stable interindividual differences. Measurements during wakefulness and in anesthesia in nine cats showed that although anesthesia lowered the absolute HVR it had no influence on the range or the rank of the magnitude of the response of individuals in the group. We observed a positive correlation between ventilatory and carotid sinus nerve (CSN) responses to hypoxia measured during anesthesia in 51 cats (r = 0.63, P less than 0.001). To assess the translation of peripheral chemoreceptor activity into expiratory minute ventilation (VE) we used an index relating the increase of VE to the increase of CSN activity for a given hypoxic stimulus (delta VE/delta CSN). Comparison of this index for cats with lowest (n = 5, HVR A = 7.0 +/- 0.8) and cats with highest (n = 5, HVR A = 53.2 +/- 4.9) ventilatory responses showed similar efficiency of central translation (0.72 +/- 0.06 and 0.70 +/- 0.08, respectively). These results indicate that interindividual variation in HVR is associated with comparable variation in hypoxic sensitivity of carotid bodies. Thus differences in peripheral chemoreceptor sensitivity may contribute to interindividual variability of HVR.


1991 ◽  
Vol 71 (3) ◽  
pp. 641-647 ◽  
Author(s):  
T. E. Michaels ◽  
D. W. Stanley

Storage of common bean (Phaseolus vulgaris L.) in elevated temperature and/or humidity conditions leads to a textural defect where the beans harden and fail to soften upon soaking and cooking. The objectives of this study were to determine the stability of 20 common bean cultivars grown in three environments for initial hardness, final hardness following storage and hardening ratio, and to estimate the heritability of these hardening parameters. Cultivar × environment interaction was highly significant for the hardening parameters. When stability was examined by plotting hardness against coefficient of variation across environments, three cultivars, GN-77135B, ICA Pijao and T39 Black Turtle, were marginally below the mean for both final hardness and coefficient of variation. While the coefficients of variation for the red kidney bean cultivars Redkloud and Montcalm were high, the maximum compression forces were only slightly (< 20%) greater than the maximum acceptable hardness level as determined by a sensory panel. Fiesta Pinto had the lowest coefficient of variation and near mean values for both final hardness and hardening ratio making it arguably the cultivar with best combination of texture and stability. Heritability estimates were low (0–0.24) with high standard error and estimates of the proportion of phenotypic variance due to G × E were moderate to high (0.29–0.69). Initial cultivar improvement efforts should focus on developing cultivars with greater stability across environments for the hardening parameters. Key words: Phaseolus vulgaris L., storage-induced hardening, stability, broad sense heritability, bean (common)


2000 ◽  
Vol 88 (5) ◽  
pp. 1907-1914 ◽  
Author(s):  
Dean M. Robinson ◽  
Henry Kwok ◽  
Brandon M. Adams ◽  
Karen C. Peebles ◽  
Gregory D. Funk

We examined developmental changes in breathing pattern and the ventilatory response to hypoxia (7.4% O2) in unanesthetized Swiss CD-1 mice ranging in age from postnatal day 0 to 42(P0–P42) using head-out plethysmography. The breathing pattern of P0 mice was unstable. Apneas were frequent at P0 (occupying 29 ± 6% of total time) but rare by P3 (5 ± 2% of total time). Tidal volume increased in proportion to body mass (∼10–13 ml/kg), but increases in respiratory frequency (f) (55 ± 7, 130 ± 13, and 207 ± 20 cycles/min for P0, P3, and P42, respectively) were responsible for developmental increases in minute ventilation (690 ± 90, 1,530 ± 250, and 2,170 ± 430 ml ⋅ min− 1 ⋅ kg− 1for P0, P3, and P42, respectively). Between P0 and P3, increases in f were mediated by reductions in apnea and inspiratory and expiratory times; beyond P3, increases were due to reductions in expiratory time. Mice of all ages showed a biphasic hypoxic ventilatory response, which differed in two respects from the response typical of most mammals. First, the initial hyperpnea, which was greatest in mature animals, decreased developmentally from a maximum, relative to control, of 2.58 ± 0.29 in P0 mice to 1.32 ± 0.09 in P42mice. Second, whereas ventilation typically falls to or below control in most neonatal mammals, ventilation remained elevated relative to control throughout the hypoxic exposure in P0 (1.73 ± 0.31), P3 (1.64 ± 0.29), and P9 (1.34 ± 0.17) mice but not in P19 or P42 mice.


2000 ◽  
Vol 88 (4) ◽  
pp. 1421-1430 ◽  
Author(s):  
G. Kim Prisk ◽  
Ann R. Elliott ◽  
John B. West

We measured the isocapnic hypoxic ventilatory response and the hypercapnic ventilatory response by using rebreathing techniques in five normal subjects (ages 37–47 yr) before, during, and after 16 days of exposure to microgravity (μG). Control measurements were performed with the subjects in the standing and supine postures. In both μG and in the supine position, the hypoxic ventilatory response, as measured from the slope of ventilation against arterial O2 saturation, was greatly reduced, being only 46 ± 10% (μG) and 52 ± 11% (supine) of that measured standing ( P < 0.01). During the hypercapnic ventilatory response test, the ventilation at a[Formula: see text] of 60 Torr was not significantly different in μG (101 ± 5%) and the supine position (89 ± 3%) from that measured standing. Inspiratory occlusion pressures agreed with these results. The findings can be explained by inhibition of the hypoxic but not hypercapnic drive, possibly as a result of an increase in blood pressure in carotid baroreceptors in μG and the supine position.


1978 ◽  
Vol 45 (6) ◽  
pp. 971-977 ◽  
Author(s):  
George D. Swanson ◽  
Brian J. Whipp ◽  
Robert D. Kaufman ◽  
Kamel A. Aqleh ◽  
Benjamin Winter ◽  
...  

Steplike end-tidal hypoxic drives (Petcoco2, = 53 Torr) lasting for 5 min were generated in a group of normal subjects and a group of carotid body-resected subjects when end-tidal CO2, was maintained constant under eucapnic (Petcoco2 = 39 Torr) and hypercapnic (Petcoco2 = 49 Torr) conditions. The hypoxic ventilatory response of the normal subjects was prompt and significant in eucapnia and was enhanced in the hypercapnic state, evidencing CO2-O2 interaction. In contrast, the carotid body-resected subjects did not respond to eucapnic hypoxia but did demonstrate a small but significant ventilatory response to hypoxia against the hypercapnic background. This suggests that the aortic bodies in man may contribute a small component of the hypoxic ventilatory drive under hypercapnic conditions, although the possibility of neuromalike ending regeneration cannot be excluded.


2019 ◽  
Vol 131 (3) ◽  
pp. 467-476 ◽  
Author(s):  
Suzanne J. L. Broens ◽  
Martijn Boon ◽  
Chris H. Martini ◽  
Marieke Niesters ◽  
Monique van Velzen ◽  
...  

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background The ventilatory response to hypoxia is a life-saving chemoreflex originating at the carotid bodies that is impaired by nondepolarizing neuromuscular blocking agents. This study evaluated the effect of three strategies for reversal of a partial neuromuscular block on ventilatory control in 34 healthy male volunteers on the chemoreflex. The hypothesis was that the hypoxic ventilatory response is fully restored following the return to a train-of-four ratio of 1. Methods In this single-center, experimental, randomized, controlled trial, ventilatory responses to 5-min hypoxia (oxygen saturation, 80 ± 2%) and ventilation at hyperoxic isohypercapnia (end-tidal carbon dioxide concentration, 55 mmHg) were obtained at baseline, during rocuronium-induced partial neuromuscular block (train-of-four ratio of 0.7 measured at the adductor pollicis muscle by electromyography), and following reversal until the train-of-four ratio reached unity with placebo (n = 12), 1 mg neostigmine/0.5 mg atropine (n = 11), or 2 mg/kg sugammadex (n = 11). Results This study confirmed that low-dose rocuronium reduced the ventilatory response to hypoxia from 0.55 ± 0.22 (baseline) to 0.31 ± 0.21 l · min−1 · %−1 (train-of-four ratio, 0.7; P &lt; 0.001). Following full reversal as measured at the thumb, there was persistent residual blunting of the hypoxic ventilatory response (0.45 ± 0.16 l · min−1 · %−1; train-of-four ratio, 1.0; P &lt; 0.001). Treatment effect was not significant (analysis of covariance, P = 0.299) with chemoreflex impairment in 5 (45%) subjects following sugammadex reversal, in 7 subjects (64%) following neostigmine reversal, and in 10 subjects (83%) after spontaneous reversal to a train-of-four ratio of 1. Conclusions Despite full reversal of partial neuromuscular block at the thumb, impairment of the peripheral chemoreflex may persist at train-of-four ratios greater than 0.9 following reversal with neostigmine and sugammadex or spontaneous recovery of the neuromuscular block.


1978 ◽  
Vol 44 (3) ◽  
pp. 464-468 ◽  
Author(s):  
C. H. Scoggin ◽  
R. D. Doekel ◽  
M. H. Kryger ◽  
C. W. Zwillich ◽  
J. V. Weil

One difference between endurance athletes and nonathletes is decreased ventilatory responsiveness to hypoxia and hypercapnia. It has never been clear whether these decreased responses are a consequence of conditioning or precede participation in endurance athletics. Recent studies demonstrating clusters of decreased ventilatory responses to hypoxia in families of patients with unexplained respiratory failure suggest that decreased responses in endurance athletes might be familial. To investigate this possibility, ventilatory response to hypoxia and hypercapnia were measured in 16 nonathletic, healthy parents and siblings of five successful long-distance runners. Response were compared to 34 nonathletic controls. As measured by the shape parameter A, hypoxic response was decreased to a similar extent in runners 74 +/- 6.4 (mean +/- SE) (P less than 0.05) and their relatives 69 +/- 15.2 (P less than 0.01) compared to control 128 +/- 11.3. Hypercapnic responses were slightly, but not significantly, decreased in runners and their families. We conclude familial influences made a major contribution to the decreased hypoxic ventilatory response seen in long-distance runners.


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