Pulmonary circulation and gas exchange at exercise in Sherpas at high altitude

Faoro, Vitalie; Huez, Sandrine; Vanderpool, Rebecca; Groepenhoff, Herman; Bisschop, Claire de; Martinot, Jean-Benoît; Lamotte, Michel; Pavelescu, Adriana; Guénard, H.; Naeije, Robert

doi:10.1152/japplphysiol.00236.2013

Cited by 49 publications

(42 citation statements)

References 29 publications

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“…After correction, PASP in Sherpa fell within sea level norms at ~24mmHg therefore indicating that hematocrit and subsequently viscosity are predominantly responsible for their elevated PASP at 5050m. This further provides evidence suggesting a differential regulation of PASP between lowlanders and high altitude natives, and indicates that we and others 28,29,48 have likely underestimated the difference in HPV between lowlanders and Sherpa without consideration of changes in HCT 33 .…”

Section: Discussionsupporting

confidence: 61%

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Hoiland

Foster

Donnelly

et al. 2015

Chest

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Abstract:The hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA), HVR at SL may not predict PASP at HA. We hypothesized that resting peripheral oxyhemoglobin saturation (SpO 2 ) at HA would correlate better than HVR at SL to PASP at HA. In 20 participants at SL, we measured normobaric, isocapnic HVR (L/min·-%SpO 2 -1 ) and resting PASP using echocardiography.Both resting SpO 2 and PASP measures were repeated on day 2 (n=10), days 4-8 (n=12), and 2-3 weeks (n=8) after arrival at 5050m. These data were also collected at 5050m on life-long HA residents (Sherpa; n=21

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Section: Discussionsupporting

confidence: 61%

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Hoiland

Foster

Donnelly

et al. 2015

Chest

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“…However, we calculated PVR for a standardized haematocrit of 45% (Faoro et al . ). By accounting for this 2% difference in haematocrit, we would observe a PVR of 1.38 and 1.40 in control and AZ.…”

Section: Discussionmentioning

confidence: 97%

Hypoxia, not pulmonary vascular pressure, induces blood flow through intrapulmonary arteriovenous anastomoses

Tremblay

Lovering

Ainslie

et al. 2014

The Journal of Physiology

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Key pointsr Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased by acute hypoxia during rest by unknown mechanisms.r Oral administration of acetazolamide blunts the pulmonary vascular pressure response to acute hypoxia, thus permitting the observation of IPAVA blood flow with minimal pulmonary pressure change.r Hypoxic pulmonary vasoconstriction was attenuated in humans following acetazolamide administration and partially restored with bicarbonate infusion, indicating that the effects of acetazolamide on hypoxic pulmonary vasoconstriction may involve an interaction between arterial pH and P CO 2 .r We observed that IPAVA blood flow during hypoxia was similar before and after acetazolamide administration, even after acid-base status correction, indicating that pulmonary pressure, pH and P CO 2 are unlikely regulators of IPAVA blood flow.Abstract Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased with exposure to acute hypoxia and has been associated with pulmonary artery systolic pressure (PASP). We aimed to determine the direct relationship between blood flow through IPAVA and PASP in 10 participants with no detectable intracardiac shunt by comparing: (1) isocapnic hypoxia (control); (2) isocapnic hypoxia with oral administration of acetazolamide (AZ; 250 mg, three times a day for 48 h) to prevent increases in PASP; and (3) isocapnic hypoxia with AZ and 8.4% NaHCO 3 infusion (AZ + HCO 3 -) to control for AZ-induced acidosis. Isocapnic hypoxia (20 min) was maintained by end-tidal forcing, blood flow through IPAVA was determined by agitated saline contrast echocardiography and PASP was estimated by Doppler ultrasound. Arterial blood samples were collected at rest before each isocapnic-hypoxia condition to determine pH, and P a,CO 2 . AZ decreased pH (-0.08 ± 0.01), (−7.1 ± 0.7 mmol l −1 ) and P a,CO 2 (−4.5 ± 1.4 mmHg; P < 0.01), while intravenous NaHCO 3 restored arterial blood gas parameters to control levels. Although PASP increased from baseline in all three hypoxic conditions (P < 0.05), a main effect of condition expressed an 11 ± 2% reduction in PASP from control (P < 0.001) following AZ administration while intravenous NaHCO 3 partially restored the PASP response to isocapnic hypoxia. Blood flow through IPAVA increased during exposure to isocapnic hypoxia (P < 0.01) and was unrelated to PASP, cardiac output and pulmonary vascular resistance for all conditions. In conclusion, isocapnic hypoxia induces blood flow through IPAVA independent of changes in PASP and the influence of AZ on the PASP response to isocapnic hypoxia is dependent upon the H + concentration or P a,CO 2 .

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“…A blunted pulmonary vascular response in Tibetans (and Sherpas) has also been found in exercise studies at altitude [24] and in comparison with acclimatised lowlanders and Quechuas from the Andes [21]. In peripheral blood lymphocytes in Tibetans, the expression and hypoxic induction of HIF-regulated genes was lower than in the Han Chinese [23].…”

Section: Biological Significance Of Hpvmentioning

confidence: 62%

“…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. There are many physiological adaptations (erythropoiesis, ventilatory drive and angiogenesis, and notably an increased transfer factor for carbon monoxide and nitric oxide [21]) all linked to the hypoxia-inducible factor (HIF) family of genes and to cellular hypoxia (see [22] for an overview).…”

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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Pulmonary circulation and gas exchange at exercise in Sherpas at high altitude

Cited by 49 publications

References 29 publications

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Hypoxia, not pulmonary vascular pressure, induces blood flow through intrapulmonary arteriovenous anastomoses

Hypoxic pulmonary vasoconstriction: clinical implications

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