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Altitude, temperature, circadian rhythms and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Henning Wackerhage, Kenneth A. Dyar, Martin Schönfelder
At high altitude, people are exposed to chronic hypoxia. For example, if the barometric pressure at sea level is 760 mmHg then the inspired partial pressure of oxygen (PIO2) will be 149 mmHg, 101 mmHg in a settlement at 3,000 m, 89 mmHg at 4,000 m and 78 mmHg at 5,000 m. Such hypoxia is a great challenge to the human body and of the more than 140 million people that live above 250 m, 5–10% are at risk of developing chronic mountain sickness. Chronic mountain sickness is a major health problem which is associated with a high haemoglobin concentration and haematocrit, a reduced oxygen saturation and often a high blood pressure in the lung circuit, termed pulmonary hypertension (22). Thus, the questions are: Are populations that live permanently at high altitudes genetically adapted to chronic hypoxia? Do they carry DNA sequence variants such as those possessed by a Finnish family, where a heterozygous EPO receptor gene (EPOR) mutation increased haematocrit (23)?
High altitude residents
Published in Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson, Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson
As is the case with lowland populations, highland residents are at a growing risk for a variety of noncommunicable diseases including various forms of cardiovascular diseases, cancer, chronic respiratory diseases, and diabetes mellitus. Historically, high altitude regions have been associated with decreased access to medical resources, which can affect the burden of and outcomes from these and other noncommunicable diseases, although many of these access issues may be changing as a result of increasing levels of development, migration, and greater ease of travel to and from these regions. In this section, mortality from noncommunicable diseases specific to indigenous high altitude populations is reviewed followed by a discussion of several specific noncommunicable diseases. Chronic mountain sickness, a major form of noncommunicable disease in many high altitude regions, is discussed in Chapter 24.
Rheology of Polycythemias T. C. Pearson
Published in Gordon D. O. Lowe, Clinical Blood Rheology, 2019
In the habitual mountain dweller with the excessive polycythemia of Monge’s disease, the changes in pulmonary hemodynamics are similar to those seen in chronic hypoxic lung disease.42 Normally, pulmonary artery pressures are greater in healthy high altitude residents than those found in sea level dwellers. In Monge’s disease, these pressures are about twice those of the healthy high altitude residents. This pulmonary hypertension results from a combination of arteriolar vasoconstriction due to hypoxia and increased blood viscosity, which may be very high since PCV values are in the order of 0.70 to 0.80. A study of venesection in six patients with chronic mountain sickness has been reported.42 Reduction of PCV from 0.72 to 0.66 led to an increase in arterial oxygen saturation and some reduction in pulmonary artery pressure. These results suggested that the hyperviscosity was probably contributing independently to some of the hemodynamic changes.
Nocturnal hypoxemia, blood pressure, vascular status and chronic mountain sickness in the highest city in the world
Published in Annals of Medicine, 2022
Elisa Perger, Sébastien Baillieul, François Esteve, Aurélien Pichon, Gzregorz Bilo, Davide Soranna, Stéphane Doutreleau, Yann Savina, Mathilde Ulliel-Roche, Julien V. Brugniaux, Emeric Stauffer, Laura Oberholzer, Connor Howe, Ivan Hannco, Carolina Lombardi, Renaud Tamisier, Jean-Louis Pepin, Samuel Verges, Gianfranco Parati
In response to chronic hypobaric hypoxia, permanent high-altitude residents develop physiological adaptations. Despite these adaptations, chronic mountain sickness (CMS) can be observed in 5%–33% of highlanders [1,2]. CMS is a syndrome defined by excessive erythrocytosis (EE; haemoglobin concentration, [Hb] ≥ 21 g dL−1 for males), associated with signs and symptoms such as breathlessness, palpitations, dizziness, sleep disturbance, cyanosis, peripheral vein dilatation, headache and tinnitus [2]. CMS is often associated with cardiorespiratory diseases such as pulmonary hypertension, right or left heart failure and systemic arterial dysfunction [3]. Although genetic and systemic pathophysiological alterations have been proposed as potential causes of respiratory, cardiovascular, and hormonal responses to chronic hypoxaemia [4–6], the exact mechanisms underlying EE and CMS are still not completely understood.
Physiological variations among blood parameters of domestic cats at high- and low-altitude regions of China
Published in Archives of Physiology and Biochemistry, 2018
Hui Zhang, Hailong Dong, Khalid Mehmood, Kun Li, Fazul Nabi, Zhenyu Chang, Mujeeb Ur Rehman, Muhammad Ijaz, Qingxia Wu, Jiakui Li
Tibet is geographically isolated from Sichuan and other provinces by the Himalayas and it shares border with Yunnan and Qinghai Provinces (Zhang et al.2014). The average elevation of the surveyed area is more than 3100 m above the sea level, which induce high-altitude hypoxic conditions (Zhang et al.2017a, 2017b, Rehman et al.2017). Tibetan cats are exposed to low-oxygen environment in this region; however, they have a strong resistance to chronic mountain sickness (Zhang et al.2007). Bar-headed geese (Anserindicus) are commonly found on the Tibetan Plateau, which migrates from low to high elevated regions and had a high-oxygen affinity and invariable values of red blood cells (RBCs), haematocrit (HCT), haemoglobin (HGB) and mean corpuscular volume (MCV) concentration at high-altitude region (Black and Tenney 1980). Genetic modifications in haemoglobin enable the increase affinity of blood-O2 for the adaptation of vertebrates at high-altitude hypoxic environments (Janecka et al.2015). Ye et al. (1994) reported that highland native animals had higher RBCs numbers and lower MCV contents, which advantageous their oxygen transport. The objective of this study was to determine the physiological changes in blood of semi-long-haired Tonkinese cat breed (called as Tibetan cats) at both high and low altitudes. The findings of present study mainly attribute towards compensatory modifications or possible adaptation of Tibetan cats to high-altitude hypoxic conditions.
Apoptosis is one cause of thrombocytopenia in patients with high-altitude polycythemia
Published in Platelets, 2023
Zhuoya Wang, Noryung Tenzing, Qiying Xu, Huifang Liu, Yi Ye, Yi Wen, Tana Wuren, Sen Cui
There are 140 million people living in the highlands around the world [1]. People who are intolerant to hypoxia may suffer from chronic mountain sickness that is characterized by high-altitude polycythemia (HAPC; females Hb 19 g/dL; males Hb 21 g/dL), with an incidence of 5%–10% [2]. Hypoxic environments inhabited by patients with HAPC transform blood into a hypercoagulable state, thereby increasing the risk of arteriovenous thrombosis [3–7]. Antithrombotic therapy is the primary treatment option for these patients, but caution is warranted in some cases, including thrombocytopenia. A meta-analysis of the effects of high altitude exposure on platelet counts (PCs) showed that acute hypoxia had no significant effect on PCs, but chronic hypoxia, especially in patients with high altitude polycythemia, had a significant decrease in PCs [8]. Therefore, understanding thrombocytopenia can lead to improved treatment outcomes when using antithrombotic drugs. If platelet output is reduced, anticoagulation and antiplatelet therapy should be used with caution, as patients may experience excessive bleeding. There are several pathological states, including disseminated intravascular coagulation, sepsis, and rheumatoid arthritis, in which PC also decreases. These effects are partly related to excessive platelet activation and subsequent platelet consumption [9,10]. Procoagulant platelets, which are essential for clot formation, can undergo apoptosis or necrosis [11–13]. If thrombocytopenia in HAPC patients is closely related to platelet activation, anticoagulation and antiplatelet therapy should be sufficient to inhibit thrombosis and relieve thrombocytopenia.