High-altitude illness: Management approach

Aksel, Gökhan; Çorbacıoğlu, Şeref Kerem; Özen, Can

doi:10.1016/j.tjem.2019.09.002

Cited by 33 publications

(26 citation statements)

References 60 publications

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“…Hypoxia is the most critical cause of acute mountain sickness (AMS) [1,2]. At high-altitude environments (above 2,500 meters) air oxygen levels remain constant, but as the altitude increases the oxygen partial pressure (PaO2) drops [3,4]. In non-acclimatized individuals, this reduction in PaO2 can cause arterial desaturation or hypoxemia, which restricts the diffusion of oxygen into alveolar capillaries and lung tissue and may lead to lifethreatening conditions, i.e.…”

Section: Introductionmentioning

confidence: 99%

“…In non-acclimatized individuals, this reduction in PaO2 can cause arterial desaturation or hypoxemia, which restricts the diffusion of oxygen into alveolar capillaries and lung tissue and may lead to lifethreatening conditions, i.e. high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE) [3,5]. Normally, the alveolar capillary barrier maintains the balance of fluid exchange in the alveoli.…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of lung miR-203a-3p expression by high-altitude hypoxia enhances VEGF/Notch signaling

Cai

Liu

et al. 2020

Aging

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Hypoxia-related microRNAs (miRNAs) are involved in the pathogenesis of various diseases. Because potential variations in miRNA expression mediated by hypoxic lung injury at high altitude remain incompletely characterized, we used a rat model to investigate the biochemical and miRNA changes induced by high-altitude hypoxia. After 24, 48, or 72 h of hypoxic exposure, expression of VEGF/Notch pathway-related proteins were increased in rat lung tissues. Microarray screening of hypoxic lung samples revealed 57 differentially expressed miRNAs, 19 of which were related to the VEGF/Notch signaling pathway. We verified that the top downregulated miRNA (miR-203a-3p) suppresses VEGF-A translation through direct binding and also indirectly reduces Notch1, VEGFR2, and Hes1 levels, which restricts the angiogenic capacity of pulmonary microvascular endothelial cells in vitro. These findings may aid in the development of new therapeutic strategies for the prevention and treatment of hypoxic lung injury at high altitude.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Downregulation of lung miR-203a-3p expression by high-altitude hypoxia enhances VEGF/Notch signaling

Cai

Liu

et al. 2020

Aging

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“…A considerable proportion of people who live in plains will suffer from high-altitude illnesses when they suddenly ascend to an altitude of over 2,500 m without acclimatization, such as acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema (HACE; Aksel et al, 2019 ). Moreover, multiple physiologic changes occur during exposure to hypoxia for acclimatization that impacts the cardiovascular system.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Perturbed Cardiac Metabolism in Rats Under High-Altitude Hypoxia by Combination Treatment With L-carnitine and Trimetazidine

Xie

et al. 2021

Front. Physiol.

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High-altitude hypoxia has long been recognized as a vital etiology for high-altitude illnesses. High-altitude myocardial injury (HAMI) usually occurs in people who suffered from high-altitude exposure. To date, the molecular mechanism of HAMI remains elusive, which seriously hinders the prevention and treatment of HAMI. L-carnitine and trimetazidine are classic cardiovascular protective medicines. In this study, we used the metabolomic method, based on GC/MS, to explore the changes in metabolites in rats exposed to high-altitude hypoxia and then illustrate the metabolic pathways associated with the modulatory effect of L-carnitine combined with trimetazidine on rats with high-altitude exposure. The results showed that metabolites in the myocardium in rats under high-altitude hypoxia were markedly changed, such as branched-chain amino acids (BCAA, leucine, isoleucine, and valine), taurine, succinic acid, fumaric acid, lactic acid, pyruvic acid, 3-hydroxybutyrate, and docosahexaenoic acid (DHA), while L-carnitine combined with trimetazidine modulated and improved the abnormal changes in energy substances caused by high-altitude hypoxia. L-carnitine mainly promoted the metabolism of fatty acids, while trimetazidine enhanced the glycolysis process. The combined administration of the two components not only increased the metabolism of fatty acids but also promoted aerobic glycolysis. Meanwhile, it contributed to the decrease in the elevation in some of the intermediates of the tricarboxylic acid (TCA) cycle, decrease in the production of 3-hydroxybutyric acid, and relief of the abnormal energy metabolism process in organisms and the cardiac tissue. Our analysis delineates the landscape of the metabolites in the myocardial tissue of rats that were exposed to high altitude. Moreover, L-carnitine combined with trimetazidine can relieve the HAMI through modulated and improved abnormal changes in energy substances caused by high-altitude hypoxia.

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“…Although AMS is not often life threatening, it may significantly affect the work efficacy and cognitive function for workers and travelers. So many studies focus on the prophylaxis and therapy of AMS (Li et al, 2018, Aksel et al, 2019.…”

Section: Introductionmentioning

confidence: 99%

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2021

Pak. J. Pharm. Sci

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Severe oxidative stress triggered by acute hypobaric hypoxia (AHH) is harmful for lots of organs in body, especial brain and heart. Flavonoids with antioxidant properties can protect organs from oxidative stress. Our previous study found that 5,6,7,6,7,, a flavones with four consecutive hydrogen group on ring A, showed excellent antioxidant properties in vitro. In the present study, the protective of 5,6,7,8-THF against oxidative stress caused by AHH was investigated. Mice were administered with 5,6,7,8-THF(500mg/kg) for 5 consecutive days before HH exposure. The heart rate (HR) and blood pressure (BP) was measured. The activity of SOD, CAT, GSH-Px, LDH, Na + -K + -ATPase and Ca 2+ -Mg 2+ -ATPase and the content of H 2 O 2 , MDA, LD and ATP in brain and heart tissue was evaluated using commercial kit. AHH led to a significant increase in HR and decrease in BP. Pretreatment of 5,6,7,8-THF could reversed these changes. In addition, administration of 5,6,7,8-THF could significantly increase the activity of SOD, CAT and GSH-Px and decrease the content of H 2 O 2 and MDA in the brain and heart of mice under AHH. Furthermore, 5,6,7,8-THF inhibited the activity of LDH, decreased the level of LD and improved ATPase activity. These results indicate that 5,6,7,8-THF may protect the mice against AHH injury via scavenging free radical, inhibiting lipid peroxidation, enhancing antioxidant enzyme activity, preserving energy metabolism and can be further explored as an excellent anti-hypoxia agent for preventing acute mountain sickness.

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High-altitude illness: Management approach

Cited by 33 publications

References 60 publications

Downregulation of lung miR-203a-3p expression by high-altitude hypoxia enhances VEGF/Notch signaling

Downregulation of lung miR-203a-3p expression by high-altitude hypoxia enhances VEGF/Notch signaling

Modulation of Perturbed Cardiac Metabolism in Rats Under High-Altitude Hypoxia by Combination Treatment With L-carnitine and Trimetazidine

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