hypocapnia/hypoxia

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Role of the central and arterial chemoreceptors in the response of gastric tone and motility to hypoxia, hypercapnia and hypocapnia in rats.

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The contribution of autonomic nerve activity to stomach tone and motility during central and arterial chemoreceptor excitation or inhibition was analyzed in urethane anesthetized, artificially ventilated rats. Systemic severe hypoxia at end-tidal O2 concentration (FETO2) 6% and systemic hypercapnia

[Interrelations of hypocapnia, hypoxia, cerebral blood flow and electrical activity of the brain under voluntary hyperventilation in humans].

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Changes of different physiological parameters in human caused by hyperventilation of 3-min and longer duration were investigated and correlated. It was found that during 3-min hyperventilation, resulting in 4.5-5 fold increase of the respiration velocity, similar phasing changes of the central and

Hypoxia, hypocapnia and spirometry at altitude.

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1. Both hypoxia and hypocapnia can cause broncho-constriction in humans, and this could have a bearing on performance at high altitude or contribute to altitude sickness. We studied the relationship between spirometry, arterial oxygen saturation and end-tidal carbon dioxide (ETCO2) concentration in

Interaction of hypocapnia, hypoxia, brain blood flow, and brain electrical activity in voluntary hyperventilation in humans.

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Changes in various physiological measures in voluntary hyperventilation lasting three minutes or more in humans were studied and compared. Three-minute hyperventilation, in which the rate of external ventilation increased by an average factor of 4.5-5, produced similar phasic changes in central and

Ventilatory effects of specific carotid body hypocapnia and hypoxia in awake dogs.

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Specific carotid body (CB) hypocapnia in the-10-Torr (less than eupneic) range reduced ventilation in the awake and sleeping dog to the same degree as did CB hyperoxia [CB PO2 (PCBO2); > 500 Torr; C.A. Smith, K.W. Saupe, K. S. Henderson, and J. A. Dempsey. J. Appl. Physiol. 79:689-699, 1995],

Influences on the cardiovascular response to graded levels of systemic hypoxia of the accompanying hypocapnia in the rat.

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1. In spontaneously breathing, anaesthetized rats, a study was made of the effects upon the graded cardiovascular responses to systemic hypoxia (inspiratory fractional O2 concentration, Fi, O2: 0.15, 0.12, 0.08, 0.06) of maintaining arterial CO2 pressure (Pa,CO2) at the air-breathing level by adding

Physiological dead space increases during initial hours of chronic hypoxemia with or without hypocapnia.

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A whole body plethysmograph was used to determine the minute ventilation-to-CO2 production ratio (VE/VCO2) of intact unrestrained unanesthetized adult male Sprague-Dawley rats during 7 days of hypoxemia (arterial PO2 approximately 50 Torr). In one set of rats, normocapnia (arterial PCO2

Effects of moderate hypoxemia and hypocapnia on CSF [H+] and ventilation in man.

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The effects of 26 h of normoxic hypocapnia (PaCO2, 31 MMHg) vs. 26 h of hypocapnia plus hypobaric hypoxia (PaCO2 32, PaO2 57 mmHg) were compared with respect to: a) CSF acid-base status; and b) the spontaneous ventilation (at PIO2 145 mmHg) which followed the imposed (voluntary) hyperventilation.

Hypocapnia increases the prevalence of hypoxia-induced augmented breaths.

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Augmented breaths promote respiratory instability and have been implicated in triggering periods of sleep-disordered breathing. Since respiratory instability is well known to be exacerbated by hypocapnia, we asked whether one of the destabilizing effects of hypocapnia might be related to an

[Regulative role of hypocapnia on cerebral blood flow under hypoxia in rats].

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The experiments were performed on urethane anesthetized and artificially ventilated SD rats using a gascous mixture of 11.9% O2 and 88.1% N2. The PaCO2 was regulated by changing the volume of ventilation. The items to be studies are: (1) The correlation between hypocapnia and CBF under hypoxia; (2)

Effects of hypoxia and hypocapnia on brain redox balance in ducks.

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Low arterial CO2 tension (PaCO2) experienced by birds during high-altitude flight may result in cerebral vasoconstriction with reduced cerebral O2 delivery. To test this, brain redox balance and blood volume were studied during severe hypocapnia (PaCO2 11-20 mmHg) in ducks. Cerebrocortical redox

Hypocapnia and sustained hypoxia blunt ventilation on arrival at high altitude.

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Hypoxia at high altitude stimulates ventilation, but inhibitory influences in the first days after arrival limit the ventilatory response. Possible inhibitory influences include hypocapnia and depression of ventilation during sustained hypoxia. Our approach was to compare hypoxic ventilatory

Slow V˙O2 kinetics in acute hypoxia are not related to a hyperventilation-induced hypocapnia.

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We examined whether slower pulmonary O2 uptake (V˙O2p) kinetics in hypoxia is a consequence of: a) hypoxia alone (lowered arterial O2 pressure), b) hyperventilation-induced hypocapnia (lowered arterial CO2 pressure), or c) a combination of both. Eleven participants performed 3-5 repetitions of

Somatosensory evoked potentials during hypoxia and hypocapnia in conscious humans.

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OBJECTIVE The objective of the study was to evaluate the effects of moderate hypoxia and hypocapnia on the latency and amplitude of cortical somatosensory evoked potentials (SSEPs) in conscious human subjects. METHODS In ten volunteers the amplitude and latency of the cortical somatosensory evoked

Difference in glossopharyngeal and phrenic inspiratory activities of rats during hypocapnia and hypoxia.

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Inspiratory (I) activities of glossopharyngeal (IX) and phrenic (Phr) nerves were compared during hypocapnia or hypoxia in the urethane anesthetized and carotid deafferented rat. Hypoxic or hypocapnic suppression of I activity was smaller in the IX than in the Phr nerve. A small ramp like rhythmic

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