Humans In Hypoxia: A Conspiracy Of Maladaptation?!

Dempsey, Jerome A.; Morgan, Barbara J.

doi:10.1152/physiol.00007.2015

Cited by 74 publications

(78 citation statements)

References 134 publications

(108 reference statements)

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“…In this part of the curve the gradient of a few mm Hg in the inhaled air can cause significant changes in oxygen supply slowing down ATP synthesis that is a direct destructive effect. As Dempsey and Morgan [6] have written in their last review, the sigmoid shape of the HbO 2 disassociation curve permits substantial (up to one-third) reductions from the normal arterial PO 2 before serious reductions occur in arterial O 2 saturation and content and therefore in O 2 transport. In the range of 80 to 50 mm Hg, there is such a degree of hypoxia when the supply of reduced coenzymes in the electron transport chain of mitochondria slows down.…”

Section: Regimes Of Iht With Hypoxic Gas Mixtures Inhalation: Recommementioning

confidence: 99%

“…Powerful hypoxic-induced gene transcription factors (HIF-1/HIF-2 alpha) are activated very early upon hypoxic exposure, guaranteeing time-dependent up-regulation of cardiorespiratory and hematological responses aimed at limiting deficits in O 2 transport [62]. As Dempsey and Morgan [6] have written, on the adaptive side, short-term exposures (via manipulation of FiO 2 ) to a few weeks of daily sessions consisting of 10-15 1-to 2-min bouts of moderate isocapnic hypoxemia (SpO 2 75-80%) alternating with equal durations of normoxia have been shown to yield several benefits without maladaptive consequence.…”

Section: Regimes Of Iht With Hypoxic Gas Mixtures Inhalation: Recommementioning

confidence: 99%

“…Mechanisms of maladaptive responses are very good described in recent reviews [6,54,62,71,72, and many others]. Studies in this field have led to the view that intermittent hypoxia is the principal, if not the only, risk factor for the development of a number of detrimental cardiovascular, respiratory, metabolic, and cognitive outcomes [7].…”

Section: Potential Side Effectsmentioning

confidence: 99%

“…This topic is the subject of many articles, reviews and monographs. To avoid repetition we refer readers to the most recent reviews [3][4][5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Fitness and therapeutic potential of intermittent hypoxia training: a matter of dose

Serebrovska¹,

Serebrovska²,

Egorov³

2016

Fiziol Zh

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Section: Regimes Of Iht With Hypoxic Gas Mixtures Inhalation: Recommementioning

confidence: 99%

Section: Regimes Of Iht With Hypoxic Gas Mixtures Inhalation: Recommementioning

confidence: 99%

Section: Potential Side Effectsmentioning

confidence: 99%

“…This topic is the subject of many articles, reviews and monographs. To avoid repetition we refer readers to the most recent reviews [3][4][5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Fitness and therapeutic potential of intermittent hypoxia training: a matter of dose

Serebrovska¹,

Serebrovska²,

Egorov³

2016

Fiziol Zh

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“…HPV is switched off at birth, but responds in adult life to external (high-altitude) or internal (local hypoventilation) hypoxia. The disadvantage of HPV in those who live, work and perform athletic training at altitude is the extra load incurred by the right ventricle [19] from the pulmonary hypertension induced by exercise in hypoxia [20]. There is considerable interest currently in how populations that have lived at altitudes >4300 m, either in the Tibetan or the Andean (Quechua and Aymara residents) plateaus have adapted with success to chronic hypoxia.…”

Section: Biological Significance Of Hpvmentioning

confidence: 99%

Hypoxic pulmonary vasoconstriction: clinical implications

Hughes

2015

Eur Respir J

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@ERSpublicationsHPV is an adaptation for fetal development and affords some advantage in optimising gas exchange in adults http://ow.ly/Uh54oHypoxic pulmonary vasoconstriction (HPV) and its mechanism of action continue to be of great interest to clinicians and physiologists. SOMMER et al. Fetal origin of HPVHPV originates in the fetus [3]. Vasomotor tone can be detected in the human fetal pulmonary circulation in the last trimester of pregnancy [4]. HPV contributes significantly to the high pulmonary vascular resistance (PVR) in the fetus (only 10-15% of right ventricular outflow goes to the lungs) [5], mainly because pulmonary artery and alveolar fluid oxygen tension (PO 2 ) levels are considerably lower (18 mmHg) than they are after birth; also, the fetal pulmonary arteries are more muscularised (this regresses in the neonatal period). The low PO 2 in the fetal pulmonary artery, versus that in the fetal aorta, is due to "streaming" in the right ventricle, whereby oxygen-poor blood from the tissues enters via the superior vena cava and is directed to the pulmonary circulation; oxygen-enriched blood (via the placental vein) enters from the inferior vena cava and passes into the left ventricle via the foramen ovale.At birth, the lungs expand with air from the first breath, alveolar liquid is reabsorbed, the alveolar PO 2 (PAO 2 ) increases dramatically, which reduces HPV, and vasodilators such as nitric oxide and prostacyclin (also called prostaglandin I 2 (PGI 2 )) are synthesised and released [5]. All these factors combine to reduce PVR five-fold (for a review, see GAO and RAJ [3]). Pulmonary artery pressure falls from about 50 to 20 mmHg and pulmonary blood flow increases three-fold. This remarkable transition at birth is, in large part, due to the inhibition of HPV. HPV clearly has a role to play in the latter third of fetal development in helping to adjust the distribution of the combined ventricular outputs in the most favourable manner for organ growth and development. HPV occurs in almost all vertebrates [1]. How useful or otherwise is its persistence into post-natal life? HPV in the normal post-natal lungIn adult mammals, the pulmonary arteriolar ( pre-acinar) vessels constrict when local PAO 2 is reduced, and dilate when it increases. This occurs over a wide PAO 2 range, from 40 to 150 mmHg [6,7]. The response is attenuated by local hypocapnia [8] or a rise in pulmonary artery pressure [9], and is augmented by a rise in local carbon dioxide tension (PCO 2 ) [8]. In experimental models (dog [10] or sheep [8]), inspired PO 2 was lowered in one or more lobes and blood flow diversion measured. With a calculated reduction in alveolar ventilation (V′A) of 70%, affecting 10-20% of total lung units, HPV reduced local blood flow by 45-50% [8,10]. If 50% of the lung was "hypoxic", the reduction was 30% [8], presumably because of the attenuating

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