Hypoxic depression of ventilation in humans: alternative models for the chemoreflexes

Khamnei, Saeed; Robbins, Peter A.

doi:10.1016/0034-5687(90)90074-9

Cited by 65 publications

(58 citation statements)

References 20 publications

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“…In both groups the change in ventilation was achieved predominantly by increments in the neuro-muscular drive (VTÏTI) with smaller changes in central timing (TIÏTtot) though, in both groups, the change remained within range one of the Clark-Von Euler diagram (Clark & Von Euler, 1972). The ventilatory responses of the young group were similar to the results reported by Khamnei & Robbins (1989, 1990) and more recently by Poulin et al (1993). Ahmed et al (1991) described the response to sustained isocapnic hypoxia in an 'older' group, however their subjects were nearly 12 years younger than the old group in this study.…”

Section: Discussionsupporting

confidence: 77%

Dynamic Ventilatory Response to Acute Isocapnic Hypoxia in Septuagenarians

Smith

Poulin

Paterson

et al. 2001

Experimental Physiology

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This study compared the ventilatory response to 20 min of acute isocapnic hypoxia (end‐tidal PO2, 50 mmHg) using the technique of dynamic end‐tidal forcing in young (Y) and old (O) men. Two groups of non‐smoking male subjects (mean ± s.d. age: Y, 29.8 ± 6.9 years; O, 73.4 ± 2.8 years) with similar body size, normal age‐predicted spirometry, and normal moderate levels of physical activity were studied. Compared with baseline ventilation in euoxia (10.79 ± 1.99 and 11.88 ± 0.91 l min−1) both groups responded to the abrupt onset of isocapnic hypoxia with peak ventilatory responses of 22.58 ± 2.60 and 24.56 ± 2.54 l min−1 for Y and O, respectively (not significant, n.s.). Both groups demonstrated a significant increment in neuromuscular drive (i.e. tidal volume (VT)/inspiratory time (TI); 0.46 ± 0.06 to 0.91 ± 0.15 and 0.48 ± 0.06 to 0.91 ± 0.12 l s−1 for Y and O, respectively) with a small (but also significant) change in central timing (TI/total ventilation time (Ttot); 0.38 ± 0.02 to 0.41 ± 0.02 and 0.42 ± 0.02 to 0.45 ± 0.02 for Y and O, respectively). Oxygen sensitivity was assessed using Weil's equation, and gave a hyperbolic factor (A) of 282 ± 75 and 317 ± 72, and using the linear equation: change in expiratory minute volume (ΔVE)/change in arterial O2 saturation (ΔSa,O2) which gave ‐1.17 ± 0.57 and ‐1.17 ± 0.42 l min−1%−1 (n.s.) for Y and O, respectively. After 20 min of sustained isocapnic hypoxia, ventilation declined to 14.29 ± 1.92 and 16.85 ± 2.34 l min−1 for Y and O, respectively (n.s.). The acute response to hypoxia was characterised by similar time constants (16.0 ± 5.4 and 18.5 ± 6.7 s) and time delays (4.8 ± 2.1 and 4.6 ± 1.9 s) for Y and O, respectively. Thus, the dynamic ventilatory response to acute isocapnic hypoxia is maintained into the eighth decade in a group of habitually active elderly men.

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Section: Discussionsupporting

confidence: 77%

Dynamic Ventilatory Response to Acute Isocapnic Hypoxia in Septuagenarians

Smith

Poulin

Paterson

et al. 2001

Experimental Physiology

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“…In response to hypoxic challenge, ventilation was first augmented and then gradually depressed but still remaining higher than during the hyperoxic period, as demonstrated previously (Easton et al 1986;Khamnei & Robbins, 1988). On the other hand, no apparent change in Q was elicited by hypoxic exposure.…”

supporting

confidence: 72%

Proceedings of the Physiological Society, 30 June‐ 1 July 1989, Oxford Meeting: Communications

1989

The Journal of Physiology

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“…However, we found the opposite in our experiments since after hypoxia the normoxic ventilation was about 2 1 min' higher (Table 2). Several investigators have noted a gradual increase of ventilation during hypercapnia (Georgopoulos et al 1989 a;Khamnei & Robbins, 1990). The mechanism of this gradual increase is unknown but seems to go hand in hand with an increase in both SP and S, ( (Lahiri & DeLaney, 1975).…”

Section: Protocol Imentioning

confidence: 99%

“…In adult human beings the ventilatory response to isocapnic sustained hypoxia is a rapid increase in ventilation (VI) followed by a slow decline (Weiskopf & Gabel, 1975;Weil & Zwillich, 1976; Kagawa, Stafford, Waggener & Severinghaus, 1982;Easton, Slykerman & Anthonisen, 1986; Nishimura, Suzuki, Nishiura, Yamamoto, A. BERKENBOSCH AND OTHERS Miyamoto, Kishi & Kawakami, 1987;Khamnei & Robbins, 1990). The rapid increase in ventilation is due to the peripheral drive from the carotid bodies.…”

Section: Introductionmentioning

confidence: 99%

The ventilatory response to CO2 of the peripheral and central chemoreflex loop before and after sustained hypoxia in man.

Berkenbosch

Dahan

DeGoede

et al. 1992

The Journal of Physiology

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SUMMARY1.The ventilatory response to sustained hypoxia is characterized by a fast increase due to the peripheral chemoreceptors followed by a slow decline. The mechanism of this decline is unknown.2. To investigate the characteristics of the ventilatory response to sustained hypoxia ten healthy subjects were exposed to two consecutive periods of isocapnic hypoxia (arterial saturation 78%) separated by a 5 min exposure to isocapnic normoxia.3. The acute hypoxic response to the second exposure to hypoxia (mean increase in ventilation + s.E.M., 7-2 + 08 1 min') was significantly depressed (P = 004) compared to the first one (9 5 + 1-3 1 min-). 4. To investigate whether this depression was due to central or-peripheral effects or both we measured, in the same ten subjects, the normoxic ventilatory response to CO2 before and after a period of 25 min of hypoxia using the technique of dynamic end-tidal forcing.5. Each response was separated into a fast peripheral and slow central component characterized by a CO2 sensitivity, time constant, time delay and an off-set.6. A total of thirty-six prehypoxic and thirty posthypoxic responses were analysed. The ventilatory CO2 sensitivities of the peripheral and central chemoreflex loops and the overall off-set (apnoeic threshold) after 25 min of hypoxia were somewhat larger than their prehypoxic values, but this effect was not significant. 7. We argue that the hypoxic ventilatory decline in man is due to a change in the off-set of the peripheral chemoreflex loop.

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Hypoxic depression of ventilation in humans: alternative models for the chemoreflexes

Cited by 65 publications

References 20 publications

Dynamic Ventilatory Response to Acute Isocapnic Hypoxia in Septuagenarians

Dynamic Ventilatory Response to Acute Isocapnic Hypoxia in Septuagenarians

Proceedings of the Physiological Society, 30 June‐ 1 July 1989, Oxford Meeting: Communications

The ventilatory response to CO2 of the peripheral and central chemoreflex loop before and after sustained hypoxia in man.

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