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Increase in slow-wave vasomotion by hypoxia and ischemia in lowlanders and highlanders

Title: Increase in slow-wave vasomotion by hypoxia and ischemia in lowlanders and highlanders
Authors: Salvi, Paolo; Faini, Andrea; Castiglioni, Paolo; Brunacci, Fausto; Montaguti, Luca; Severi, Francesca; Gautier, Sylvie; Pretolani, Enzo; Benetos, Athanase; Parati, Gianfranco
Contributors: Salvi, P; Faini, A; Castiglioni, P; Brunacci, F; Montaguti, L; Severi, F; Gautier, S; Pretolani, E; Benetos, A; Parati, G
Publisher Information: American Physiological Society
Publication Year: 2018
Collection: Università degli Studi di Milano-Bicocca: BOA (Bicocca Open Archive)
Subject Terms: Altitude; Hypoxia; Laser-Doppler flowmetry; Microcirculation; Vasomotion
Description: The physiological relevance of slow-wave vasomotion is still unclear, even though it has been hypothesized that it could be a compensatory mechanism for enhancing tissue oxygenation in conditions of reduced oxygen supply. The aim of our study was to explore the effects of hypoxia and ischemia on slow-wave vasomotion in microcirculation. Peripheral oxygen saturation and forearm microcirculation flow (laser-Doppler flowmetry) were recorded at baseline and during postocclusive reactive hyperemia in the Himalaya region from 8 European lowlanders (6 men; aged 29-39 yr) at 1,350, 3,400, and 5,050 m and from 10 Nepalese male highlanders (aged 21-39 yr) at 3,400 and 5,050 m of altitude. The same measurements were also performed at sea level in 16 healthy volunteers (aged 23-61 yr) during a short-term exposure to normobaric hypoxia. In lowlanders, exposure to progressively higher altitude under baseline flow conditions progressively increased 0.06- 0.15 Hz vasomotion amplitude [power spectral density % was expressed as geometric means (geometric standard deviation) = 14.0 (3.6) at 1,350 m; 87.0(2.3) at 3,400 m and 249.8 (3.6) at 5,050 m; P = 0.006 and P < 0.001 vs. 1,350 m, respectively]. In highlanders, low frequency vasomotion amplitude was similarly enhanced at different altitudes [power spectral density % = 183.4 (4.1) at 3,400 m vs. 236.0 (3.0) at 5,050 m; P = 0.139]. In both groups at altitude, it was further increased after ischemic stimulus (P < 0.001). At baseline, acute short lasting normobaric hypoxia did not induce low frequency vasomotion, which was conversely induced by ischemia, even under normal oxygenation and barometric pressure. This study offers the demonstration of a significant increase in slow-wave vasomotion under prolonged hypobaric-hypoxia exposure at high altitude, with a further enhancement after ischemia induction.
Document Type: article in journal/newspaper
Language: English
Relation: info:eu-repo/semantics/altIdentifier/pmid/29927733; info:eu-repo/semantics/altIdentifier/wos/WOS:000445958900011; volume:125; issue:3; firstpage:780; lastpage:789; numberofpages:10; journal:JOURNAL OF APPLIED PHYSIOLOGY; https://hdl.handle.net/10281/216977
DOI: 10.1152/japplphysiol.00977.2017
Availability: https://hdl.handle.net/10281/216977; https://doi.org/10.1152/japplphysiol.00977.2017; https://www.physiology.org/doi/pdf/10.1152/japplphysiol.00977.2017
Rights: info:eu-repo/semantics/openAccess
Accession Number: edsbas.C3ED7D73
Database: BASE