scholarly journals High-Altitude Pulmonary Vascular Diseases

2017 ◽  
Vol 15 (3) ◽  
pp. 149-157 ◽  
Author(s):  
Maniraj Neupane ◽  
Erik R. Swenson
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Vascular Diseases ◽  
Hypoxic Exposure ◽  
Partial Pressure Of Oxygen ◽  
Chronic Mountain Sickness ◽  
Pulmonary Vasoconstriction ◽  
High Altitude Pulmonary Edema ◽  
Mountain Sickness ◽  
Pulmonary Vascular Diseases

More than 140 million people permanently reside in high-altitude regions of Asia, South America, North America, and Africa. Another 40 million people travel to these places annually for occupational and recreational reasons, and are thus exposed to the low ambient partial pressure of oxygen. This review will focus on the pulmonary circulatory responses to acute and chronic high-altitude hypoxia, and the various expressions of maladaptation and disease arising from acute pulmonary vasoconstriction and subsequent remodeling of the vasculature when the hypoxic exposure continues. These unique conditions include high-altitude pulmonary edema, high-altitude pulmonary hypertension, subacute mountain sickness, and chronic mountain sickness.

Role of sex hormones in development of chronic mountain sickness in rats

1994 ◽  
Vol 77 (1) ◽  
pp. 427-433 ◽  
Author(s):  
L. C. Ou ◽  
G. L. Sardella ◽  
J. C. Leiter ◽  
T. Brinck-Johnsen ◽  
R. P. Smith
Keyword(s):  
Gender Differences ◽  
Pulmonary Hypertension ◽  
High Altitude ◽  
Sex Hormones ◽  
Systolic Pressure ◽  
Female Rats ◽  
Hypoxic Exposure ◽  
Chronic Mountain Sickness ◽  
Mountain Sickness

After chronic exposure to hypoxia, Hilltop Sprague-Dawley rats developed excessive polycythemia and severe pulmonary hypertension and right ventricular (RV) hypertrophy, signs consistent with human chronic mountain sickness; however, there were gender differences in the magnitude of the polycythemia and susceptibility to the fatal consequence of chronic mountain sickness. Orchiectomy and ovariectomy were performed to evaluate the role of sex hormones in the gender differences in these hypoxic responses. After 40 days of exposure to simulated high altitude (5,500 m; barometric pressure of 370 Torr and inspired Po2 of 73 Torr), both sham-gonadectomized male and female rats developed polycythemia and had increased RV peak systolic pressure and RV hypertrophy. The hematocrit was slightly but significantly higher in males than in females. Orchiectomy did not affect these hypoxic responses, although total ventricular weight was less in the castrated high-altitude rats. At high altitude, the mortality rates were 67% in the sham-operated male rats and 50% in the castrated animals. In contrast, ovariectomy aggravated the high-altitude-associated polycythemia and increased RV peak systolic pressure and RV weight compared with the sham-operated high-altitude female rats. Both sham-operated control and ovariectomized females suffered negligible mortality at high altitude. The present study demonstrated that 1) the male sex hormones play no role in the development of the excessive polycythemia, pulmonary hypertension, and RV hypertrophy during chronic hypoxic exposure or in the associated high mortality and 2) the female sex hormones suppressed both the polycythemic and cardiopulmonary responses in vivo during chronic hypoxic exposure.

scholarly journals Long-term chronic intermittent hypoxia: a particular form of chronic high-altitude pulmonary hypertension

2020 ◽  
Vol 10 (1_suppl) ◽  
pp. 5-12
Author(s):  
Julio Brito ◽  
Patricia Siques ◽  
Eduardo Pena
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Intermittent Hypoxia ◽  
Clinical Presentation ◽  
Chronic Intermittent Hypoxia ◽  
Chronic Mountain Sickness ◽  
Epidemiological Pattern ◽  
Mountain Sickness

In some subjects, high-altitude hypobaric hypoxia leads to high-altitude pulmonary hypertension. The threshold for the diagnosis of high-altitude pulmonary hypertension is a mean pulmonary artery pressure of 30 mmHg, even though for general pulmonary hypertension is ≥25 mmHg. High-altitude pulmonary hypertension has been associated with high hematocrit findings (chronic mountain sickness), and although these are two separate entities, they have a synergistic effect that should be considered. In recent years, a new condition associated with high altitude was described in South America named long-term chronic intermittent hypoxia and has appeared in individuals who commute to work at high altitude but live and rest at sea level. In this review, we discuss the initial epidemiological pattern from the early studies done in Chile, the clinical presentation and possible molecular mechanism and a discussion of the potential management of this condition.

scholarly journals Echocardiographic and invasive measurements of pulmonary artery pressure correlate closely at high altitude

2000 ◽  
Vol 279 (4) ◽  
pp. H2013-H2016 ◽  
Author(s):  
Yves Allemann ◽  
Claudio Sartori ◽  
Mattia Lepori ◽  
Sébastien Pierre ◽  
Christian Mélot ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Doppler Echocardiography ◽  
Systolic Pulmonary Arterial Pressure ◽  
Wide Range ◽  
High Altitude Pulmonary Edema ◽  
Reproducible Method ◽  
Pulmonary Arterial ◽  
Spearman Test ◽  
Invasive Measurement

Exaggerated hypoxia-induced pulmonary hypertension is a hallmark of high-altitude pulmonary edema (HAPE) and plays a major role in its pathogenesis. Many studies of HAPE have estimated systolic pulmonary arterial pressure (SPAP) with Doppler echocardiography. Whereas at low altitude, Doppler echocardiographic estimation of SPAP correlates closely with its invasive measurement, no such evidence exists for estimations obtained at high altitude, where alterations of blood viscosity may invalidate the simplified Bernoulli equation. We measured SPAP by Doppler echocardiography and invasively in 14 mountaineers prone to HAPE and in 14 mountaineers resistant to this condition at 4,559 m. Mountaineers prone to HAPE had more pronounced pulmonary hypertension (57 ± 12 and 58 ± 10 mmHg for noninvasive and invasive determination, respectively; means ± SD) than subjects resistant to HAPE (37 ± 8 and 37 ± 6 mmHg, respectively), and the values measured in the two groups as a whole covered a wide range of pulmonary arterial pressures (30–83 mmHg). Spearman test showed a highly significant correlation ( r = 0.89, P < 0.0001) between estimated and invasively measured SPAP values. The mean difference between invasively measured and Doppler-estimated SPAP was 0.5 ± 8 mmHg. At high altitude, estimation of SPAP by Doppler echocardiography is an accurate and reproducible method that correlates closely with its invasive measurement.

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