Ventilatory oxygen drive in acute and chronic hypoxia

Lefrançois, R; Gauiter, H.; Pasquis, P

doi:10.1016/0034-5687(68)90053-4

Cited by 73 publications

(25 citation statements)

References 11 publications

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“…In accordance with the observations of Lefrançois et al [5], prolonged hyperoxia from the breathing of high oxygen concentrations produces ef fects not only from suppression of an oxygen drive but also from the action of changes in arterial pH, HbC>2 and Pcoa, as well as cerebral blood flow (CSF). Consequently, the 2-single-breath-C>2 test of Dejours [11] was used in this study on the assumption that this determines best the peripheral chemoreceptor-mediated oxygen drive of the 4 groups at both altitudes.…”

Section: Hypoxic Drive In the 4 Groupssupporting

confidence: 53%

“…In agreement with similar observations made by L efra n^ois el al. [5], the alveolar gas tensions of the 4 groups come to lie between the acute and acclimatized curves; the plots for A clearly follow a curve separate Fig. 18.…”

Section: Discussionmentioning

confidence: 99%

“…The respiratory sensitivity to hypoxia of high-altitude native males in the Himalayas [1,2] and the Andes [3][4][5] is reduced, contrasted with that of newcomers from sea level visiting the same altitude. Evidence of an at tenuation in hypoxic drive, which persists in highlanders after residing at sea level for 10 months, points to a possible and irreversible genetic origin for the low respiratory response to hypoxia [6], It is not known if this applies to both sexes.…”

Section: Introductionmentioning

confidence: 99%

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Respiratory Studies in Women at High Altitude (3,600 m or 12,200 ft and 5,200 m or 17,200 ft)

1972

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At two altitudes (3,600 and 5,200 m), resident native women (A) showed higher PAco₂ and Paco₂, lower PAO₂ and PaO₂, as well as lower arterial pH, than native males (C) of similar age. Resting minute ventilation (VE/m²), tidal volume (VT) and respiratory frequency (f) were similar. The differences in the alveolar-arterial gas tensions in A stem from larger dead space (VDS), VDS/VT and reduced alveolar ventilation (VA). Newcomer females (B) at both altitudes differed from new- comer males (D) in regard to larger resting VA, f and smaller VT. No differences were demonstrated in size of VDS, VDS/VT or VO₂/BSA; but PAco₂ and PacO₂ were lower, PAO₂ and Pa higher and VE/VO2 and VA/VO₂ (ventilatory equivalents) above those for resting newcomer males. A contrasted with resting B at 3,600 m (12,200 ft), showing higher PAco₂ and Paco₂, lower Pao₂ and arterial pH, reduction in VA and larger VDS/VT. Both C and D at 3,600 and 5,200 m during steady-state 60-W (367 kg/m/min) exercise showed lower PAco₂ and Paco₂, higher arterial pH, smaller VDS and higher VE/VO₂ than exercising A. The latter differed from C exercising at the same work load in that VE/m² and VA were reduced, PAco₂ and Paco₂ were higher, Pa-ao₂ gradients were wider, pH was lower and VDS as well as VDS/VT were larger. Contrasted with B during steady-state 60-W exercise at both altitudes, D showed consistently smaller VDS and larger VA. While both C and A had higher resting f than D, f of newcomer females at La Paz was higher than that of A. Control of ventilation by relating VE to Pao₂ and Paco₂ at rest and exercise at both altitudes showed marked attenuation of hypoxic and hypercapnic drives, particularly in the native resident female, suggesting diminished peripheral chemoreceptor function.

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Section: Hypoxic Drive In the 4 Groupssupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Respiratory Studies in Women at High Altitude (3,600 m or 12,200 ft and 5,200 m or 17,200 ft)

1972

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“…However, the animal species from high altitude, which have been examined, i.e. llama, dog, cat and goat do not show a decreased ventilatory response to acute hypoxia (Brooks & Tenney, 1968;Lefrancois, Gautier & Pasquis, 1968;Hornbein & Sorensen, 1969;Mines & Sorensen, 1969) though Tenney, Scotto, Ou, Bartlett & Remmers (1972) and Barer et al (1972) found a decrease in the ventilatory response to acute hypoxia in normal sea level cats and rats when they were exposed to hypoxia in a low pressure chamber for a few weeks. Thus rabbits might also show a lowered ventilatory response to hypoxia following exposure to hypoxia.…”

Section: Discussionmentioning

confidence: 97%

The ultrastructure of the carotid body in chronically hypoxic rabbits

Møller¹,

Møllgård²,

Sørensen³

1974

The Journal of Physiology

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SUMMARY1. The ultrastructure of the carotid body in the rabbit has been examined by electron microscopy.2. A comparison was made between the ultrastructure of the carotid bodies in sea level rabbits, in rabbits which had been exposed to hypoxia equivalent to an altitude of 6000 m for 7 days and in rabbits which always had lived at an altitude of 4000-4300 m.3. We could not detect any difference in the ultrastructure between the two groups of hypoxic rabbits.4. When the hypoxic rabbits were compared with sea level rabbits there was a marked increase in the number of dense cored vesicles and mitochondria in the type I cells in the hypoxic rabbits. The Golgi region also appeared to be enlarged in the type I cells in the hypoxic rabbits.5. The finding suggests that in the rabbit the production of amines, probably dopamine, within the type I cells is increased during prolonged hypoxia which might explain the lowered ventilatory response to hypoxia observed in human high altitude residents.6. If the carotid bodies are organs of internal secretion the finding is compatible with an increased production of a hormone produced within the type I cells.

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“…The O 2 gradient between atmospheric air and cells decreases from 105 mmHg at sea level to 49 mmHg at high altitude (20). There are a number of adaptive responses that are triggered by this situation, such as increased ventilation (28), pulmonary hypertension (40), erythropoiesis (39), and heart work load. The adaptation to high altitude constitutes a situation that has both advantageous and disadvantageous consequences for human health.…”

mentioning

confidence: 99%

Mitochondrial nitric oxide metabolism during rat heart adaptation to high altitude: effect of sildenafil,l-NAME, andl-arginine treatments

Zaobornyj¹,

Valdez²,

Iglesias³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Zaobornyj T, Valdez LB, Iglesias DE, Gasco M, Gonzales GF, Boveris A. Mitochondrial nitric oxide metabolism during rat heart adaptation to high altitude: effect of sildenafil, L-NAME, and L-arginine treatments. Am J Physiol Heart Circ Physiol 296: H1741-H1747, 2009. First published April 3, 2009 doi:10.1152/ajpheart.00422.2008.-Rats submitted to high altitude (Cerro de Pasco, Perú, 4,340 m, PO2 ϭ 12.2 kPa) for up to 84 days showed a physiological adaptive response with decreased body weight gain (15%), increased right ventricle weight (100%), and increased hematocrit (40%) compared with sea level animals. These classical parameters of adaptation to high altitude were accompanied by an increase in heart mitochondrial enzymes: complexes I-III activity by 34% and mitochondrial nitric oxide synthase (mtNOS) activity and expression by Ͼ75%. The hyperbolic increase for mtNOS activity during adaptation to high altitude was similar to the observed pattern for hematocrit. Hematocrit and mtNOS activity mean values correlated linearly (r 2 ϭ 0.75, P Յ 0.05). Chronic treatment for 28 days with sildenafil (50 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) decreased the response of mtNOS to high altitude by 25%. Conversely, N Gnitro-L-arginine methyl ester treatment (8.3 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) increased such response by 40%, whereas L-arginine treatment (106 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) had no effect. Nitric oxide (NO) production by mtNOS accounts for ϳ49% of total cellular NO production in sea level rats and for ϳ54% in rats exposed to high altitude for 84 days. It is concluded that mtNOS is a substantial source of cardiac NO, a factor in the adaptive response to sustained heart hypoxia that is susceptible to be modified by pharmacological treatments. mitochondrial nitric oxide synthase activity; mitochondrial nitric oxide synthase expression; mitochondrial respiratory complexes; hematocrit; nitro-L-arginine methyl ester HIGH ALTITUDE IS A MULTIFACTORIAL source of stress in which hypobaric hypoxia is the most important component. The O 2 gradient between atmospheric air and cells decreases from 105 mmHg at sea level to 49 mmHg at high altitude (20). There are a number of adaptive responses that are triggered by this situation, such as increased ventilation (28), pulmonary hypertension (40), erythropoiesis (39), and heart work load. The adaptation to high altitude constitutes a situation that has both advantageous and disadvantageous consequences for human health. The main long term effects are decreased physical activity and life span. Among the beneficial effects, there is a recognized cardioprotection with improvement of the myocardial tolerance to ischemic episodes. A number of studies involving exposure to natural (22) or simulated (29) hypobaric hypoxia reported that this adaptation is associated to lower incidence and smaller size of myocardial infarction (30).Although the mechanism by which adaptation to hypoxia has cardioprotective effects remains not elucidated, nitric oxide (NO) has been extensively proposed as one of the molecular messengers inv...

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Ventilatory oxygen drive in acute and chronic hypoxia

Cited by 73 publications

References 11 publications

Respiratory Studies in Women at High Altitude (3,600 m or 12,200 ft and 5,200 m or 17,200 ft)

Respiratory Studies in Women at High Altitude (3,600 m or 12,200 ft and 5,200 m or 17,200 ft)

The ultrastructure of the carotid body in chronically hypoxic rabbits

Mitochondrial nitric oxide metabolism during rat heart adaptation to high altitude: effect of sildenafil,l-NAME, andl-arginine treatments

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