Body fluid compartments, renal blood flow, and hormones at 6,000 m in normal subjects

Anand, Inder; Chandrashekhar, Y.; Rao, Sachin; Malhotra, Rama; Ferrari, Roberto; Chandana, Jagdish; Ramesh, Bala; Shetty, Kirti; Boparai, M. S.

doi:10.1152/jappl.1993.74.3.1234

Cited by 59 publications

(36 citation statements)

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“…Moreover, sleep curtailment can elevate the circadian trough in the cortisol profile on the following day (104). Complementary data based on observations at high altitude also show that hypoxia modifies the diurnal pattern of cortisol secretion (105)(106)(107)(108)(109)(110)(111). Thus, there is ample biological basis to speculate that apnea-related intermittent hypoxemia and recurrent arousals may negatively impact HPA function.…”

Section: The Hypothalamic-pituitary-adrenal Dysfunction As a Causal Imentioning

confidence: 97%

Sleep Apnea and Metabolic Dysfunction: Cause or Co-Relation?

Aurora

Punjabi

2007

Sleep Medicine Clinics

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Section: The Hypothalamic-pituitary-adrenal Dysfunction As a Causal Imentioning

confidence: 97%

Sleep Apnea and Metabolic Dysfunction: Cause or Co-Relation?

Aurora

Punjabi

2007

Sleep Medicine Clinics

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“…Hypoxiainduced neuroendocrine activation may also play a role. 96 The question arises of whether the exaggerated HPV observed in HAPE-susceptible individuals persists during prolonged exposure to high altitude causing SAMS. Supporting this is the similar prevalence of both illnesses: 15% for HAPE in soldiers transported rapidly to 5500 m 97 and 10% to 20% for SAMS when transported more gradually to the same altitude.…”

Section: Subacute Mountain Sicknessmentioning

confidence: 99%

Effect of Altitude on the Heart and the Lungs

2007

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T his review focuses on the effects of altitude exposure from 1 to several days or weeks as occurs in tourists, trekkers, and mountaineers who visit high altitude and normally reside near sea level. We briefly review the acute physiological adjustments and early acclimatization that occur in the cardiovascular system and the lungs of healthy individuals. These ensure life-sustaining oxygen delivery to the tissues despite a reduction in the partial pressure of inspired oxygen between 20% and 60% at 2500 and 8000 m, respectively. One of the acute adjustments, hypoxic pulmonary vasoconstriction (HPV), may be disadvantageous in those with a vigorous response and lead to 2 potentially lethal illnesses, high-altitude pulmonary edema (HAPE) and subacute mountain sickness (SAMS), which we present in more detail. Finally, on the basis of knowledge about the acute physiological adjustments and acclimatization and, when available, a review of the literature, we discuss the highaltitude tolerance of patients with coronary artery disease, congestive heart failure, arrhythmias, systemic hypertension, and pulmonary hypertension. Effects of Exposure to High Altitude on the Normal Cardiovascular System CirculationThe major effects of acute hypoxia on the heart and lung are shown in Figure 1. Hypoxia directly affects the vascular tone of the pulmonary and systemic resistance vessels and increases ventilation and sympathetic activity via stimulation of the peripheral chemoreceptors. 1 Interactions occur between the direct effects of hypoxia on blood vessels and the chemoreceptor-mediated responses in the systemic and pulmonary circulation. Unraveling the underlying mechanisms of the hypoxic vasodilatation of systemic arterioles is an active area of research. Several mechanisms appear to regulate local oxygen delivery according to the needs of the tissues 2,3 ; for instance, the release of ATP from red blood cells and the generation of NO by various ways appear to regulate local oxygen delivery according to the needs of the tissue. These mechanisms may decrease with prolonged stay at high altitude when oxygen content of the blood increases because of ventilatory acclimatization, an increase in hematocrit associated with plasma volume reduction, and an increase in red blood cell mass due to erythropoiesis.Peripheral chemoreceptor afferent activity rises hyperbolically as hypoxia increases. 4 Ventilation and sympathetic activity are augmented, as demonstrated by increased urinary and plasma concentration of catecholamines 5 and skeletal muscle sympathetic activity. 6 With exposure over days to weeks, the sensitivity of the peripheral chemoreceptors to hypoxia increases, leading to further enhancement of ventilation (ventilatory acclimatization). This presumably also accounts for the further increase of sympathetic activity documented by microneurography after 3 weeks at 5200 m 6 and elevated catecholamines in urine and plasma. 5 As shown in Figure 1, there is antagonism between the direct effects of hypoxia on the resistance vessels ...

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“…Thus, it is possible that HAPE susceptible subjects after gradual ascent to high altitude and a stay there for weeks, months or years may also be prone to develop high-altitude right heart failure. Moreover, additional factors, such as increased neurohumoral activity and hypoxaemia due to subclinical pulmonary oedema following impaired diastolic left ventricular function, may also add to the pathogenesis of SMS [42].…”

Section: Effects Of Acute Exposure To High Altitudementioning

confidence: 99%

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

Maggiorini¹,

León‐Velarde²

2003

Eur Respir J

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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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Body fluid compartments, renal blood flow, and hormones at 6,000 m in normal subjects

Cited by 59 publications

References 0 publications

Sleep Apnea and Metabolic Dysfunction: Cause or Co-Relation?

Sleep Apnea and Metabolic Dysfunction: Cause or Co-Relation?

Effect of Altitude on the Heart and the Lungs

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

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