Pulmonary Hypertension on Exertion in Normal Man Living at 10,150 Feet (Leadville, Colorado)*

Vogel, John H.K.; Weaver, Walt F.; Rose, Raymond L.; Blount, S. Gilbert; Grover, Robert F.

doi:10.1159/000386136

Cited by 40 publications

(56 citation statements)

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“…per cent, which implies that the resting cardiac output of these severely hypoxic emphysematous patients is normal (Table VI). Residents at an altitude of 10,150 ft. studied by Vogel et al (1962) have a similar mean arterial oxygen saturation to that of the less hypoxic emphysematous patients of the present study (those with an arterial oxygen saturation of more than 85%). The mean a-v difference of the altitude residents is not as wide as that of the emphysematous patients, but is significantly wider than the mean for normal subjects at Denver (p<0 02, Table VI), implying that the resting cardiac output of both types of subject is lower than the normal for Denver.…”

Section: Discussionsupporting

confidence: 69%

Pulmonary Circulation in Chronic Bronchitis and Emphysema

Shaw

Grover

Reeves

et al. 1967

Survey of Anesthesiology

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Section: Discussionsupporting

confidence: 69%

Pulmonary Circulation in Chronic Bronchitis and Emphysema

Shaw

Grover

Reeves

et al. 1967

Survey of Anesthesiology

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“…Pulmonary haemodynamic measurements performed in children and young adults show persistence of elevated PAP at high altitude for weeks, months or years [44,54]. Histological examination of the pulmonary vessels in high-altitude residents, who died from causes other than CMS, show persistence of the typical foetal patterns (thickened media) [45,55].…”

Section: High-altitude Pulmonary Hypertensionmentioning

confidence: 99%

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

Maggiorini¹,

León‐Velarde²

2003

European Respiratory Journal

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High-altitude pulmonary hypertension: a pathophysiological entity to different diseases. M. Maggiorini, F. Léon-Velarde. #ERS Journals Ltd 2003. ABSTRACT: Pulmonary hypertension is a hallmark of high-altitude pulmonary oedema (HAPE) and of congestive right heart failure in subacute mountain sickness (SMS) and chronic mountain sickness (CMS) in the Himalayas and in the end-stage of CMS (Monge9s disease) in the Andes.There are studies to suggest that transmission of excessively elevated pulmonary artery pressure and/or flow to the pulmonary capillaries leading to alveolar haemorrhage is the pathophysiological mechanism of HAPE.In the Himalayas, HAPE was successfully prevented by extending the acclimatisation period from a few days to 5 weeks, however, this did not prevent the occurrence of congestive right heart failure after several weeks of stay at 6,000 m. This leads to the concept that rapid remodelling of the small precapillary arteries prevents HAPE but not the development of right heart failure in SMS and CMS.Unresponsiveness of pulmonary hypertension to oxygen at high altitude and its complete resolution only after weeks of stay at low altitude suggest that structural rather than functional changes are its pathophysiological mechanism. Since pulmonary hypertension at high altitude is the driving force leading to high-altitude pulmonary oedema and "high-altitude right heart failure" in newcomers and residents of high altitude, the authors propose to adjust current terminology accordingly. The physiological response of the pulmonary circulation to hypobaric and normobaric hypoxia is to increase pulmonary arteriolar resistance. The magnitude of hypoxic pulmonary vasoconstriction is highly variable between humans, probably based on genetics and adaptive mechanisms. Sites of hypoxic pulmonary vasoconstriction are small pulmonary arterioles and veins of a diameter of v900 mm, the veins accounting for y20% of the total increase in pulmonary vascular resistance caused by hypoxia [1,2]. The structural changes in small pulmonary arteries and veins appear to reflect this genetically based and adaptive process [3][4][5] in humans and animals. Excessive hypoxic pulmonary vasoconstriction, and thus susceptibility to develop a right heart failure within weeks at high altitude, was first described in Colorado cattle [6]. Indian soldiers stationed at an altitude between 5,800-6,700 m [7] and Han infants in Lhasa [8] develop severe congestive right heart failure within weeks or months after arrival at high altitude. An excessively elevated pulmonary artery pressure (PAP) has not only been reported to cause high altitude cor pulmonale within weeks, months, or years in newcomers, but also in high-altitude residents of the Andes and nonacclimatised climbers prone to high-altitude pulmonary oedema (HAPE) [9]. The results of these studies suggest that an excessive rise in PAP is a common denominator in HAPE [9], the syndrome described by SUI et al. [8] in infants and by ANAND et al. [7] in adults at 6,700 m and termed "subacute...

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“…In humans, large inter-individual differences exist in the magnitude of the pulmonary pressure response to hypoxia [19][20][21][22], with some subjects demonstrating exaggerated increases in pulmonary arterial pressure [23,24]. There are very few studies available in North-India where the high altitude hypertension has been focused.…”

Section: Introductionmentioning

confidence: 99%

Association of High Altitude Hypertension with Angiotensin Converting Enzyme (ACE) Gene Insertion/Deletion Polymorphism

Ch¹,

Doza²,

Kumar³

2017

UNOAJ

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The study included ACE gene I/D polymorphism and its association between high altitude hypertension. Genetic, biochemical, anthropometric and Physiometeric results were analyzed using statistical software. The results were non-significant for I/D polymorphism.Objective: ACE is the major enzyme of hypertension and with most commonly reviewed I/D polymorphism. High-altitude exposes various physiological and biochemical changes, which contributes a rise in systemic blood pressure of the body. There are very few studies available in North-India, with a core focus on the high altitude hypertension. Therefore, a current study supported an interest to find out the association of high altitude hypertension with ACE gene I/D polymorphism.Methods: to study the significant association with respect to altitude, genetic, biochemical, anthropometric and physio-metric comparison were conducted among 98 individuals where 489nbeing hypertensive patients and other half being normotensive, inclusive of both males and females. The entire results were finally examined and analyzed using statistical software SPSS 16.0 version. Results:According to study results, mean arterial blood pressure and triglycerides were significantly (p<0.05) associated with SBP among both hypertensive and normotensives. Whereas HDL, LDL-HDL ratio, CHO-HDL were significantly associated only among hypertensive, and age, PP, and SpO2 have been significantly (p<0.05) associated with SBP among normotensive, a strong predictor for SBP. Conclusion:The genotypic observations were visibly linked with the disease, however, the results were statistically non-significant (ID/DD vs. II; OR: 0.54, 95% CI: 0.20-1.44, p= 0.217). A further study with considerate knowledge of noteworthy dynamics, mainly, altitude, population size, and ethnicity are recommended.

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Pulmonary Hypertension on Exertion in Normal Man Living at 10,150 Feet (Leadville, Colorado)*

Cited by 40 publications

References 0 publications

Pulmonary Circulation in Chronic Bronchitis and Emphysema

Pulmonary Circulation in Chronic Bronchitis and Emphysema

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

Association of High Altitude Hypertension with Angiotensin Converting Enzyme (ACE) Gene Insertion/Deletion Polymorphism

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