Acclimatization to Low Oxygen Tension

Stickney, J. Clifford; Liere, Edward J. Van

doi:10.1152/physrev.1953.33.1.13

Cited by 83 publications

(14 citation statements)

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“…Growth retardation is a recognized effect of chronic hypoxia (Stickney & van Liere, 1953;Mortola, Morgan & Virgona, 1986;Eden & Hanson, 1987 b). It can be explained by inadequate lactation by the mother (see Mortola et al 1986) and by decreased appetite and food ingestion (Alippi, Barcelo, Rio & Bozzini, 1983 had been hypoxic for 5-10 weeks from birth showed a normal sensitivity to changes in Pao2-However, the latter conclusion seems at variance with their finding that at 5-10 weeks the chronically hypoxic rats showed no ventilatory response when their inspirate was reduced from 15 to 12 % 02 and only a transient increase when the inspirate was reduced to 8% 02, for this implied postnatal persistence of the central-inhibitory influence.…”

Section: Group 1 (Nb)mentioning

confidence: 99%

A study on rats of the effects of chronic hypoxia from birth on respiratory and cardiovascular responses evoked by acute hypoxia.

Thomas

Marshall

1995

The Journal of Physiology

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1. Comparative studies were performed on eighteen rats 54 days old made chronically hypoxic from birth in an hypoxic chamber at 12% 02 (CHB), and in eight weight-matched control rats (NB, 42 days old); both CHB and NB rats were anaesthetized with Saffan. 2. In NB rats, breathing 12 or 8% 02 for 5 min induced a pattern of response comparable to that described in older rats (10-11 weeks old): an initial increase and secondary fall in minute volume (VE), a fall in arterial pressure (ABP), an increase in muscle vascular conductance, while cerebral blood flow (CBF) increased at the 1st minute in six animals and fell by the 5th minute in all animals. The adenosine receptor antagonist 8-phenyltheophylline (8-PT, 10 mg kg-1) reduced the secondary fall in PE, the fall in ABP and muscle vasodilatation, indicating they were partly mediated by adenosine.3. In CHB rats breathing 12% 02, VE was higher (277 + 12 vs. 204 + 18 ml min-'), arterial partial pressures of 02 (45 + 2 vs. 88 + 3 mmHg), CO2 (32 + 1 vs. 44 + 1 mmHg) and ABP (105 + 5 vs. 131 + 5 mmHg) were lower, while muscle vascular conductance was higher (0-08 + 0.01 vs. 0 03 + 0.01 ml min-mmHg-') than in NB rats breathing air; these differences were reduced, but not abolished, when CHB rats acutely breathed air for 5 min. 4. In CHB rats, the smaller change from 12 to 8% 02 for 5 min evoked a similar pattern of response to that evoked by 8% 02 in NB rats, except that heart rate (HR) and CBF decreased progressively. However, 8-PT increased baseline VE and reduced ABP in 12 % 02 and reduced the secondary decrease in VE and HR evoked by 8 % 02, but had no effect on the fall in ABP, or change in muscle vascular conductance. 5. We propose that in CHB rats (i) there is accentuation of the components of the response to acute hypoxia (the fall in ABP, HR and CBF) that form a positive feedback loop which promotes central ventilatory depression and (ii) that adenosine exerts a tonic inhibitory influence on VE and vasodilator influence in muscle and mediates the secondary fall in VE, but not the muscle vasodilatation induced by acute hypoxia.

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Section: Group 1 (Nb)mentioning

confidence: 99%

A study on rats of the effects of chronic hypoxia from birth on respiratory and cardiovascular responses evoked by acute hypoxia.

Thomas

Marshall

1995

The Journal of Physiology

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“…Others have reported both an increase in adrenal weight and a decrease in the size of the thymus [29,33] during exposure of experimental animals to lowered barometric pressures. The adrenal weight has been stated to be a good index of adrenocortical activity in experiments of more than a few days duration [25], although some of the weight increase in severe hypoxia might be attributable to the greatly in creased vascularity which is known to occur in this condition [10,28]. In the present experiments, the adrenal glands were still heavier than in the controls for up to 5 days after the period of hypoxia.…”

Section: Discussionmentioning

confidence: 43%

“…Other quantitative studies [13] have suggested that in certain circumstances at least, cortical hormones may interfere with eosinophilotactic mecha nisms, and a similar interpretation can be placed on the observations of other investigators [1,27]. Furthermore, there is evidence that the adrenal cortex has an important role in adaptation to lowered oxygen tension [28,29] and it seems likely that the marked increase in adrenal Eosinophils and Hypoxia 37 weight at day 0 (table I) indicated hyperactivity of the adrenal cortex. Others have reported both an increase in adrenal weight and a decrease in the size of the thymus [29,33] during exposure of experimental animals to lowered barometric pressures.…”

Section: Discussionmentioning

confidence: 57%

Eosinophil Leucocytes and Recovery from Severe Hypoxia

Sibley¹,

Hudson²

1970

Acta Haematol

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“…Motor functions, such as handwriting, were also impaired but to a lesser extent, and sensory modalities were affected little if at all. Investigators have documented decrements in performance on a variety of neuropsychometric tests for cognitive and motor functions after sudden exposure to even relatively moderate hypoxia (2,000-4,500 m) (Stickney and Van Liere 1953;Ernsting 1978).…”

Section: The Brain Function In Low Oxygenmentioning

confidence: 99%

Neurodegeneration in Hypoxia: Implications in Aging

Hota

Singh

2012

Brain Aging and Therapeutic Interventions

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Hypoxia and ischemia resulting in reduced oxygen delivery to brain tissues is reported to cause neurodegeneration in both in vitro and in vivo models. Similar decrease in partial pressure of oxygen occurs on ascent to high altitude, a situation referred to as hypobaric hypoxia that limits oxygen availability to the brain. Our studies on human subjects reveal decrease in vigilance and response time along with decreased cerebral oxygenation which is both altitude and duration dependent. Alterations in evoked potentials and change in hedonic matrix were also observed following exposure to high altitude environment. Investigations in animal models exposed to simulated altitude showed occurrence of oxidative stress, neurodegeneration and memory impairment. This hypoxic response of neurons is multi-factorial and involves complex signaling pathways thereby limiting the therapeutic efficacy of several antioxidants in ameliorating hypobaric hypoxia-induced memory impairment. Animals exposed to hypobaric hypoxia show depletion in the antioxidant status along with increased free radical generation. Neuromorphological studies revealed neurodegeneration and dendritic atrophy in the hippocampus. Altered neurotransmitter synthesis, release and metabolism have also been observed along with occurrence of calcium overload in hypoxic neuronal cells. These changes in the hypoxic brain find an analogy with the aging related changes that include decreased conduction rate, generation of free radicals, protein oxidation and cellular apoptosis. Administration of N-acetyl cysteine to animals exposed to hypobaric hypoxia showed considerable improvement in memory functions along with decrease in free radical generation. Acetyl-L-Carnitine administration during hypobaric hypoxia also improved the cognitive capabilities in animal models. Our investigations revealed a multifactorial action of Acetyl-L-Carnitine that included

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Acclimatization to Low Oxygen Tension

Cited by 83 publications

References 0 publications

A study on rats of the effects of chronic hypoxia from birth on respiratory and cardiovascular responses evoked by acute hypoxia.

A study on rats of the effects of chronic hypoxia from birth on respiratory and cardiovascular responses evoked by acute hypoxia.

Eosinophil Leucocytes and Recovery from Severe Hypoxia

Neurodegeneration in Hypoxia: Implications in Aging

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