Urinary catecholamine excretion on induction to high altitude (3,658 m) by air and road

Hoon, R S; Sharma, S. C.; Balasubramanian, Vijay; Chadha, K. S.

doi:10.1152/jappl.1977.42.5.728

Cited by 18 publications

(10 citation statements)

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“…A loss of sensitivity of the sinus node secondary to excessive sympathetic neurohumoral activity has been proposed to be one of the factors at the origin of reduced LF in heart failure (5). Increased neural and humoral sympathetic activities have been reported as features of established AMS (4,11,21). We may speculate that, as in heart failure, a loss of sensitivity of the sinus node secondary to excessive and more sustained sympathetic neurohumoral activity could explain the blunted LF RR NU we observed in subjects with AMS.…”

Section: Cardiovascular Variability and Amsmentioning

confidence: 53%

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Autonomic cardiovascular regulation in subjects with acute mountain sickness

Lanfranchi¹,

Colombo²,

Cremona³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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The aims of this study were 1) to evaluate whether subjects suffering from acute mountain sickness (AMS) during exposure to high altitude have signs of autonomic dysfunction and 2) to verify whether autonomic variables at low altitude may identify subjects who are prone to develop AMS. Forty-one mountaineers were studied at 4,559-m altitude. AMS was diagnosed using the Lake Louise score, and autonomic cardiovascular function was explored using spectral analysis of R-R interval and blood pressure (BP) variability on 10-min resting recordings. Seventeen subjects (41%) had AMS. Subjects with AMS were older than those without AMS (P Ͻ 0.01). At high altitude, the lowfrequency (LF) component of systolic BP variability (LFSBP) was higher (P ϭ 0.02) and the LF component of R-R variability in normalized units (LFRRNU) was lower (P ϭ 0.001) in subjects with AMS. After 3 mo, 21 subjects (43% with AMS) repeated the evaluation at low altitude at rest and in response to a hypoxic gas mixture. LFRRNU was similar in the two groups at baseline and during hypoxia at low altitude but increased only in subjects without AMS at high altitude (P Ͻ 0.001) and did not change between low and high altitude in subjects with AMS. Conversely, LFSBP increased significantly during short-term hypoxia only in subjects with AMS, who also had higher resting BP (P Ͻ 0.05) than those without AMS. Autonomic cardiovascular dysfunction accompanies AMS. Marked LFSBP response to short-term hypoxia identifies AMS-prone subjects, supporting the potential role of an exaggerated individual chemoreflex vasoconstrictive response to hypoxia in the genesis of AMS.hypoxia; autonomic nervous system; heart rate; blood pressure ACUTE MOUNTAIN SICKNESS (AMS) is a complex syndrome characterized by headache, gastrointestinal symptoms, weakness, insomnia, and certain neurological signs, including ataxia and changes in mental status (1). It may occur in subjects ascending to Ͼ2,500 m and is reported in 53% of those at Ͼ4,000-m altitude (6,22).AMS is generally harmless and transient but may occasionally progress to the more serious life-threatening cerebral and pulmonary forms of mountain sickness, i.e., high-altitude cerebral and pulmonary edema (1, 6).The exact mechanism causing AMS is unknown, although the prevailing hypothesis points to a process within the central nervous system (1), possibly an altered adaptation to the neurohumoral and hemodynamic adjustments during hypoxia (8). A marked increase in peripheral sympathetic activity is a common feature of mountain sickness (4, 11) and has also been suggested to contribute to the genesis of high-altitude pulmonary edema (4). Whether autonomic hyperactivation may play a role in the genesis of AMS is not known.The autonomic nervous system plays a role in the modulation of the oscillatory behavior of the cardiovascular system (23, 32a). Spectral analysis of variability in the R-R interval is a recognized tool that allows quantification of the oscillatory components, which in short-term recordings appear mainly organized...

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Section: Cardiovascular Variability and Amsmentioning

confidence: 53%

“…A marked increase in peripheral sympathetic activity is a common feature of mountain sickness (4,11) and has also been suggested to contribute to the genesis of high-altitude pulmonary edema (4). Whether autonomic hyperactivation may play a role in the genesis of AMS is not known.…”

mentioning

confidence: 99%

Autonomic cardiovascular regulation in subjects with acute mountain sickness

Lanfranchi¹,

Colombo²,

Cremona³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Loeppky et al (2003) inferred higher sympathoadrenergic tone due to elevated plasma levels of plasma epinephrine in AMS following 12 h of simulated altitude exposure in a decompression chamber. Hoon et al (1976) observed a significant increase in urine catecholamine excretion in individuals with AMS following rapid transport to altitude. Interestingly, the maximal increase in catecholamine excretion occurred after a week spent at altitude where most individuals became asymptomatic.…”

Section: Discussionmentioning

confidence: 79%

“…An increase in catecholamine excretion associated with a rise in sympathetic nerve activity in response to altitude has been suggested to be involved in the development of AMS (Hoon et al 1976;Loeppky et al 2003). Loeppky et al (2003) inferred higher sympathoadrenergic tone due to elevated plasma levels of plasma epinephrine in AMS following 12 h of simulated altitude exposure in a decompression chamber.…”

Section: Discussionmentioning

confidence: 99%

“…While AMS and pulmonary edema do not appear to be necessarily linked, AMS is often observed to precede cerebral edema (Hackett and Roach 2004). Causes of AMS remain unclear, but the rise in sympathetic nerve activity associated with increased catecholamine excretion in response to altitude has been suggested to be involved in the development of AMS (Hoon et al 1976;Loeppky et al 2003). It has also been suggested that individuals with smaller increases in FEFs may have greater severity of AMS (Pollard et al 1996;Singh et al 1969).…”

Section: Introductionmentioning

confidence: 99%

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Variability in pulmonary function following rapid altitude ascent to the Amundsen–Scott South Pole station

et al. 2011

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The impact of acute altitude exposure on pulmonary function is variable. A large inter-individual variability in the changes in forced expiratory flows (FEFs) is reported with acute exposure to altitude, which is suggested to represent an interaction between several factors influencing bronchial tone such as changes in gas density, catecholamine stimulation, and mild interstitial edema. This study examined the association between FEF variability, acute mountain sickness (AMS) and various blood markers affecting bronchial tone (endothelin-1, vascular endothelial growth factor (VEGF), catecholamines, angiotensin II) in 102 individuals rapidly transported to the South Pole (2835 m). The mean FEF between 25 and 75% (FEF(25-75)) and blood markers were recorded at sea level and after the second night at altitude. AMS was assessed using Lake Louise questionnaires. FEF(25-75) increased by an average of 12% with changes ranging from -26 to +59% from sea level to altitude. On the second day, AMS incidence was 36% and was higher in individuals with increases in FEF(25-75) (41 vs. 22%, P = 0.05). Ascent to altitude induced an increase in endothelin-1 levels, with greater levels observed in individuals with decreased FEF(25-75). Epinephrine levels increased with ascent to altitude and the response was six times larger in individuals with decreased FEF(25-75). Greater levels of endothelin-1 in individuals with decreased FEF(25-75) suggest a response consistent with pulmonary hypertension and/or mild interstitial edema, while epinephrine may be upregulated in these individuals to clear lung fluid through stimulation of β(2)-adrenergic receptors.

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Evaluation of sympathoadrenal activity adrenocortical function and androgenic status in five men during a Himalayan mountaineering expedition (ascent of Mt Pabil, 7,102 m, 23,294 ft)

Guilland

Moreau

Malval

et al. 1984

Europ. J. Appl. Physiol.

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Sympathoadrenal activity, adrenocortical function and androgenic status were studied in five well-trained mountaineers during the different phases of a mountaineering expedition during the ascent of Mt Pabil (7,102 m) in the Ganesh Himal massif. Sympathoadrenal activity was evaluated by measuring urinary excretion of adrenaline, noradrenaline, metanephrines, and vanillinmandelic acid. Adrenocortical function was assessed by measuring urinary excretion of free cortisol, 17 OHCS (17-hydroxycorticosteroids) and androgenic status by measuring testosterone glucuronide, Adiol (5 alpha-androstane-3 alpha, 17 beta diol) and 17KS (17-ketosteroids). Reference values were obtained at Chamonix at 1,037 m during rest. During trekking noradrenaline increased significantly while Adiol and 17-KS decreased. The fall in the urinary androgenic pool persisted during the next phases of the expedition. At base camp (4,800 m) noradrenaline, its metabolites and free cortisol increased mainly during physical activity. Above 6,000 m, adrenaline, noradrenaline, their metabolites, free cortisol and 17-OHCS reached a maximum value. During the return to sea level, the urinary level of these parameters was still high. The drop in the urinary androgenic pool observed during trekking and exposure to high altitude confirms results obtained in other studies on prolonged efforts. This hypoandrogenicity may play an important role in the metabolic adaptations as well as in the mental state of the climbers. The increase of sympathoadrenal activity and of adrenocortical function may be considered as a regulatory element in the adaptative response to hypoxia and other stressors proper to high altitude.

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Urinary catecholamine excretion on induction to high altitude (3,658 m) by air and road

Cited by 18 publications

References 0 publications

Autonomic cardiovascular regulation in subjects with acute mountain sickness

Autonomic cardiovascular regulation in subjects with acute mountain sickness

Variability in pulmonary function following rapid altitude ascent to the Amundsen–Scott South Pole station

Evaluation of sympathoadrenal activity adrenocortical function and androgenic status in five men during a Himalayan mountaineering expedition (ascent of Mt Pabil, 7,102 m, 23,294 ft)

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