Global REACH 2018

Tremblay, Joshua C.; Hoiland, Ryan L.; Howe, Connor A.; Coombs, Geoff B.; Vizcardo‐Galindo, Gustavo; Figueroa-Mujíca, Rómulo; Bermudez, Daniela; Gibbons, Travis D.; Stacey, Benjamin S.; Bailey, Damian Miles; Tymko, Michael M.; MacLeod, David B.; Gasho, Chris; Villafuerte, Francisco C.; Pyke, Kyra E.; Ainslie, Philip N.

doi:10.1161/hypertensionaha.119.12780

Cited by 51 publications

(20 citation statements)

References 70 publications

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“…The pathophysiology of HACE is reversible, and vasogenic brain edema leads to microbleeds. The collapse of the blood brain barrier due to vasodilation with increased cerebral blood flow under low oxygen pressure and high-altitude erythrocytosis causes unique distributions and distinct MRI findings ( 7 , 8 ). These structures are anatomically classified as white matter, which is more vulnerable to vasogenic brain edema in comparison to gray matter.…”

Section: Discussionmentioning

confidence: 99%

Improved Neuroimaging Findings and Cognitive Function in a Case of High-altitude Cerebral Edema

et al. 2021

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High-altitude cerebral edema (HACE) is a rare condition of acute mountain sickness that manifests as consciousness disturbance and truncal ataxia. Neuroimaging shows vasogenic edema with microbleeds in the white matter and the corpus callosum. We herein report a case of HACE in which the patient showed widespread hyperintense signals with extensive microbleeds in the white matter and corpus callosum on MRI, as well as cognitive dysfunction. Rehabilitation to improve the higher brain function facilitated the recovery of the patient's cognitive impairment and was accompanied by improved MRI findings.

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Section: Discussionmentioning

confidence: 99%

Improved Neuroimaging Findings and Cognitive Function in a Case of High-altitude Cerebral Edema

et al. 2021

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“…At 5100 m, blood viscosity measured at native haematocrit and at the two highest shear rates was higher in highlanders with moderate-to-severe CMS than in highlanders without CMS, suggesting that blood viscosity could also play a role in the development of CMS. A rise in blood viscosity has previously been observed in Andeans with EE (Tremblay et al 2019) but the relationship between CMS symptoms and blood viscosity has not yet been studied. Surprisingly, blood viscosity measured at the lower shear rate (i.e.…”

Section: Haemorheologymentioning

confidence: 99%

Blood viscosity and its determinants in the highest city in the world

Stauffer

Loyrion

Hancco

et al. 2020

The Journal of Physiology

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Key points Highlanders develop unique adaptative mechanisms to chronic hypoxic exposure, including substantial haemoglobin and haematocrit increases. However, a significant proportion of populations living permanently at high altitude develop maladaptive features known as chronic mountain sickness (CMS). This study aimed to assess the effects of permanent life at high altitude on clinical and haemorheological parameters (blood viscosity and red blood cell aggregation) and to compare clinical and haemorheological parameters of dwellers from the highest city in the world according to CMS severity. Blood viscosity increased with altitude, together with haemoglobin concentration and haematocrit. At 5100 m, highlanders with moderate‐to‐severe CMS had higher blood viscosity mainly at high shear rate and even at corrected haematocrit (40%), with a lower red blood cell aggregation. Blood viscosity may contribute to CMS symptomatology but the increased blood viscosity in CMS patients cannot solely be explained by the rise in haematocrit. Abstract Chronic mountain sickness (CMS) is a condition characterised by excessive erythrocytosis (EE). While EE is thought to increase blood viscosity and subsequently to trigger CMS symptoms, the exact relationship between blood viscosity and CMS symptoms remains incompletely understood. We assessed the effect of living at high altitude on haemoglobin, haematocrit and haemorheological parameters (blood viscosity and red blood cell aggregation), and investigated their relationship with CMS in highlanders living in the highest city in the world (La Rinconada, Peru, 5100 m). Ninety‐three men participated in this study: 10 Caucasian lowlanders, 13 Andean highlanders living at 3800 m and 70 Andean highlanders living at 5100 m (35 asymptomatic, CMS score ≤5; 15 with mild CMS, CMS score between 6 and 10; 20 with moderate‐to‐severe CMS, CMS score >10). Blood viscosity was measured at native and corrected haematocrit (40%). Haemoglobin concentration and haematocrit increased with the altitude of residency. Blood viscosity also increased with altitude (at 45 s−1: 6.7 ± 0.9 mPa s at sea level, 14.0 ± 2.0 mPa s at 3800 m and 27.1 ± 8.8 mPa s at 5100 m; P < 0.001). At 5100 m, blood viscosity at corrected haematocrit was higher in highlanders with moderate‐to‐severe CMS (at 45 s−1: 18.9 ± 10.7 mPa s) than in highlanders without CMS (10.2 ± 5.9 mPa s) or with mild CMS (12.1 ± 6.1 mPa s) (P < 0.05). In conclusion, blood viscosity may contribute to CMS symptomatology but the increased blood viscosity in CMS patients cannot solely be explained by the rise in haematocrit.

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“…It is well known that remarkable alterations occur in hematology to accommodate the HAH condition (Berglund, 1992;Huang et al, 2017). Chronic HAH-induced excessive erythrocytosis increases the blood viscosity, leading to the increased risk of various cardiovascular disorders (e.g., hypertension, vascular thrombosis, and myocardial infarction; Lowe et al, 1997;Tremblay et al, 2019). Our hematological indices revealed that chronic HAH for 4 weeks increased the amounts of overall RBCs and hemoglobin as well as the volume percentage of RBCs in the blood.…”

Section: Discussionmentioning

confidence: 68%

“…Migrants ascending to high altitudes often suffer from acute mountain sickness with symptoms, like headache, insomnia, and fatigue (Hackett and Roach, 2001), while native or longtime dwellers at high altitudes have a high risk of developing chronic mountain sickness due to compensatory adaptation of organism to chronic HAH, and the risk is greater as the altitude increases (Azad et al, 2017). Exaggerated polycythemia represent the key characteristic of acclimation to chronic HAH, which is associated with increased blood viscosity and blood volume (León-Velarde and Richalet, 2006;Tremblay et al, 2019). Long-term HAH exposure also results in pulmonary hypertension with increased pulmonary vascular resistance due to pulmonary vasoconstriction and vascular remodeling (Penaloza and Arias-Stella, 2007).…”

Section: Introductionmentioning

confidence: 99%

Oxygen Enrichment Ameliorates Cardiorespiratory Alterations Induced by Chronic High-Altitude Hypoxia in Rats

et al. 2021

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Chronic high-altitude hypoxia (HAH) results in compensatory pathological adaptations, especially in the cardiorespiratory system. The oxygen enrichment technology can provide long-lasting oxygen supply and minimize oxygen toxicity, which has proven to be effective to increase oxygen saturation, decrease heart rate, and improve human exercise performance after ascending to high altitudes. Nevertheless, it remains unknown whether oxygen enrichment can resist chronic HAH-induced cardiorespiratory alterations. Thirty-six male rats were equally assigned to the normal control (NC), HAH, and HAH with oxygen enrichment (HAHO) groups. The HAH and HAHO rats were housed in a hypobaric hypoxia chamber equivalent to 5,000 m for 4 weeks. The HAHO rats were exposed to oxygen-enriched air for 8 h/day. We found that oxygen enrichment mitigated the augmented skin blood flow and improved the locomotor activity of HAH-exposed rats. Oxygen enrichment inhibited HAH-induced increase in the production of red blood cells (RBCs). The hemodynamic results showed that oxygen enrichment decreased right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP) in HAH-exposed rats. HAH-associated right ventricular hypertrophy and cardiomyocyte enlargement were ameliorated by oxygen enrichment. Oxygen enrichment inhibited HAH-induced excessive expression of cytokines associated with cardiac hypertrophy and myocardial fibrosis [angiotensin-converting enzyme (ACE)/angiotensin-converting enzyme 2 (ACE2), angiotensin II (Ang II), collagen type I alpha 1 (Col1α1), collagen type III alpha 1 (Col3α1), and hydroxyproline] in the right ventricle (RV). Oxygen enrichment inhibited medial thickening, stenosis and fibrosis of pulmonary arterioles, and cytokine expression related with fibrosis (Col1α1, Col3α1, and hydroxyproline) and pulmonary vasoconstriction [endothelin-1(ET-1)] in HAH-exposed rats. This study represents the first effort testing the efficacy of the oxygen enrichment technique on cardiopulmonary structure and function in chronic HAH animals, and we found oxygen enrichment has the capability of ameliorating chronic HAH-induced cardiopulmonary alterations.

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Global REACH 2018

Cited by 51 publications

References 70 publications

Improved Neuroimaging Findings and Cognitive Function in a Case of High-altitude Cerebral Edema

Improved Neuroimaging Findings and Cognitive Function in a Case of High-altitude Cerebral Edema

Blood viscosity and its determinants in the highest city in the world

Oxygen Enrichment Ameliorates Cardiorespiratory Alterations Induced by Chronic High-Altitude Hypoxia in Rats

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