Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Altitude”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed2003

Influence of altitude exposure on coronary flow reserve.

BACKGROUND: Although no data exist on the effect of altitude exposure on coronary flow reserve (CFR), patients with coronary artery disease (CAD) are advised not to exceed moderate altitudes of approximately 2500 m above sea level. We studied the influence of altitude on myocardial blood flow (MBF) in controls and CAD patients. METHODS AND RESULTS: In 10 healthy controls and 8 patients with CAD, MBF was measured by positron emission tomography and 15O-labeled water at rest, during adenosine stress, and after supine bicycle exercise. This protocol was repeated during inhalation of a hypoxic gas mixture corresponding to an altitude of 4500 m (controls) and 2500 m (CAD). Workload was targeted to comparable heart rate-blood pressure products at normoxia and hypoxia. Resting MBF increased significantly in controls at 4500 m (+24%, P<0.01) and in CAD patients at 2500 m (+24%, P<0.05). Altitude had no influence on adenosine-induced hyperemia and CFR. Exercise-induced hyperemia increased significantly in controls (+38%, P<0.01) at 4500 m (despite a reduction in workload, -28%, P<0.0001) but not in CAD patients at 2500 m (moderate decrease in workload, -11%, P<0.05). Exercise-induced reserve was preserved in controls (+10%, P=NS) but decreased in CAD patients (-18%, P<0.005). CONCLUSIONS: At 2500 m altitude, there is a significant decrease in exercise-induced reserve in CAD patients, indicating that compensatory mechanisms might be exhausted even at moderate altitudes, whereas healthy controls have preserved reserve up to 4500 m. Thus, patients with CAD and impaired CFR should be cautious when performing physical exercise even at moderate altitude.

Adult↗
PubMed2000

Cerebral autoregulation in subjects adapted and not adapted to high altitude.

BACKGROUND AND PURPOSE: Impaired cerebral autoregulation (CA) from high-altitude hypoxia may cause high-altitude cerebral edema in newcomers to a higher altitude. Furthermore, it is assumed that high-altitude natives have preserved CA. However, cerebral autoregulation has not been studied at altitude. METHODS: We studied CA in 10 subjects at sea level and in 9 Sherpas and 10 newcomers at an altitude of 4243 m by evaluating the effect of an increase of mean arterial blood pressure (MABP) with phenylephrine infusion on the blood flow velocity in the middle cerebral artery (Vmca), using transcranial Doppler. Theoretically, no change of Vmca in response to an increase in MABP would imply perfect autoregulation. Complete loss of autoregulation is present if Vmca changes proportionally with changes of MABP. RESULTS: In the sea-level group, at a relative MABP increase of 23+/-4% during phenylephrine infusion, relative Vmca did not change essentially from baseline Vmca (2+/-7%, P=0.36), which indicated intact autoregulation. In the Sherpa group, at a relative MABP increase of 29+/-7%, there was a uniform and significant increase of Vmca of 24+/-9% (P<0.0001) from baseline Vmca, which indicated loss of autoregulation. The newcomers showed large variations of Vmca in response to a relative MABP increase of 21+/-6%. Five subjects showed increases of Vmca of 22% to 35%, and 2 subjects showed decreases of Vmca of 21% and 23%. CONCLUSIONS: All Sherpas and the majority of the newcomers showed impaired CA. It indicates that an intact autoregulatory response to changes in blood pressure is probably not a hallmark of the normal human cerebral vasculature at altitude and that impaired CA does not play a major role in the occurrence of cerebral edema in newcomers to the altitude.

Adaptation, Physiological↗
PubMed1992

Operation Everest II: arterial oxygen saturation and sleep at extreme simulated altitude.

Frequent sleep disturbances and desaturation during sleep are common at high altitude, but few data are available from the highest altitudes at which humans are known to sleep. Because sleep fragmentation at low altitude may impair mental function and oxygen deprivation produces lasting central nervous system abnormalities, a better understanding of the severity of sleep disturbances and oxygen desaturation at extreme altitudes is important. The purpose of this study was to determine the severity of sleep disturbance and the extent of arterial oxygen desaturation at extreme simulated altitude. Out of eight healthy male subject volunteers who started, five aged 27.2 +/- 1.5 yr completed the study during 6 weeks of progressive hypobaric hypoxia in a decompression chamber. The men were studied at barometric pressures of 760, 429, 347, 282 mm Hg and following return to 760 mm Hg. All demonstrated frequent nighttime awakenings (37.2 awakenings per subject per night at 282 mm Hg, decreasing significantly to 14.8 on return to sea level, p less than 0.05). Total sleep time decreased from 337 +/- 30 min at 760 mm Hg to 167 +/- 44 min at 282 mm Hg (p less than 0.01). Rapid eye movement (REM) sleep decreased from 17.9% +/- 6.0% of sleep time at sea level to 4.0% +/- 3.3% at 282 mm Hg (p less than 0.01). Sleep continuity as reflected by brief arousals increased from 22 +/- 6 arousals per hour of sleep at sea level to 161 +/- 66 arousals per hour at 282 mm Hg (p less than 0.01). All subjects showed arterial oxygen desaturation proportional to the altitude. The average oxygen saturation (SaO2) was 79% +/- 3% at 429 mm Hg, 66% +/- 6% at 347 mm Hg, and 52% +/- 2% at 282 mm Hg. Sleep stage had only a minimal effect on SaO2 at any altitude. SaO2 was negatively correlated with brief sleep arousals, r = -0.72, p less than 0.01. All subjects demonstrated periodic breathing with apneas throughout much of the night at 347 and 282 mm Hg. These data indicate that sleep quality progressively worsens as SaO2 decreases despite lack of progressive changes in sleep stages at altitude. This study extends previous information on the severity of desaturation during sleep, and suggests that improvements in oxygenation might prove beneficial in restoring consolidated sleep, possibly even improving daytime performance.

Adult↗
PubMed1992

Ventilation and gaseous metabolism in infants born at high altitude, and their responses to hyperoxia.

Hyperventilation and decreased metabolic rate are commonly observed in newborns during acute hypoxia; whether these responses are also present during sustained hypoxia is not known. We asked whether infants at high altitude had higher ventilation and lower metabolism than lowlanders. Ventilation (VE), oxygen consumption (VO2), and carbon dioxide production (VCO2) were measured in newborn (< 1 day old) full-term infants in La Paz (altitude 3,800 m; inspired oxygen pressure [PIO2], 92 mm Hg) and in Santa Cruz (altitude, 400 m; PIO2, 141 mm Hg), Bolivia. Each group consisted of 30 infants selected to have similar body weight. The mothers, Amerindians and mestizos, were born in the corresponding cities or at equivalent altitudes. Despite the lower inspired oxygen concentration in La Paz (0.107 ml STPD O2/ml BTPS air) than in Santa Cruz (0.164), neither VE nor VO2 or VCO2 differed between the two groups. The breathing pattern was deeper and slower at high altitude. From the values of VE and VO2 it was calculated that high-altitude infants extracted more O2 (+62%) from the inspired air than did the lowlanders. When given pure O2 to breathe, both groups of infants similarly increased VE and gaseous metabolism; even during hyperoxia, however, the ventilatory O2 extraction was higher (+50%) in the highlanders. We conclude that, contrary to what is observed in acute hypoxia, infants at high altitude maintain metabolic rate with no major alterations in VE. The ability to use a greater fraction of the inspired O2 at high altitude probably results from functional and structural alterations stimulated by fetal hypoxia.

Altitude↗
PubMed2004

Sildenafil inhibits altitude-induced hypoxemia and pulmonary hypertension.

Exposure to high altitude induces pulmonary hypertension that may lead to life-threatening conditions. In a randomized, double-blind, placebo-controlled study, the effects of oral sildenafil on altitude-induced pulmonary hypertension and gas exchange in normal subjects were examined. Twelve subjects (sildenafil [SIL] n = 6; placebo [PLA] n = 6) were exposed for 6 days at 4,350 m. Treatment (3 x 40 mg/day) was started 6 to 8 hours after arrival from sea level to high altitude and maintained for 6 days. Systolic pulmonary artery pressure (echocardiography) increased at high altitude before treatment (+29% versus sea level, p < 0.01), then normalized in SIL (-6% versus sea level, NS) and remained elevated in PLA (+21% versus sea level, p < 0.05). Pulmonary acceleration time decreased by 27% in PLA versus 6% in SIL (p < 0.01). Cardiac output and systemic blood pressures increased at high altitude then decreased similarly in both groups. Pa(O(2)) was higher and alveolar-arterial difference in O(2) lower in SIL than in PLA at rest and exercise (p < 0.05). The altitude-induced decrease in maximal O(2) consumption was smaller in SIL than in PLA (p < 0.05). Sildenafil protects against the development of altitude-induced pulmonary hypertension and improves gas exchange, limiting the altitude-induced hypoxemia and decrease in exercise performance.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1999

Effect of cold exposure, exercise and high altitude on plasma endothelin-1 and endothelial cell markers in man.

The aims were to examine the effect of cold exposure, exercise and high altitude on plasma concentrations of big endothelin-1, endothelin-1, von Willebrand factor and serum e-selectin in twenty five healthy male volunteers. Clinical evaluation and venesection were performed before and after 24 hours of low altitude mountaineering, exposure to temperatures of -18 degrees C and +4 degrees C and whilst ascending from sea level to an altitude of 5000 m in the Karakoram. Plasma big endothelin-1, plasma endothelin-1 and serum soluble e-selectin concentrations were significantly elevated after two hours at -18 degrees C (p < 0.05, p < 0.05 and p < 0.01 respectively). At +4 degrees C, plasma big endothelin-1 and endothelin-1 concentrations rose significantly after 5 hours (p < 0.005 for both) but not after 2.5 hours. Low altitude mountaineering did not alter circulating marker concentrations. At high altitude, big endothelin-1 and endothelin-1 (p < 0.01 for both) rose significantly at 2500 m and initially at 5000 m but returned to sea level values after prolonged exposure to 5000 m. Serum e-selectin rose at all altitudes greater than sea level (p < 0.05). In conclusion, exposure to high altitude, moderate cold or freezing temperatures, but not exercise, selectively activates endothelial cells increasing endothelin-1 production. Cold exposure may contribute to the observed increase in plasma endothelin-1 in mountaineers at high altitude.

Adult↗
PubMed2005

Lung function in adults with cystic fibrosis at altitude: impact on air travel.

Current guidelines for air travel state that patients with chronic respiratory diseases are required to use oxygen if their in-flight arterial oxygen tensions (Pa,O2) drop below 6.6 kPa. This recommendation may not be strictly applicable to cystic fibrosis patients, who may tolerate lower Pa,O2 for several hours without clinical symptoms. Lung function, symptoms, blood gas levels and signs of pulmonary hypertension were studied in 36 cystic fibrosis patients at altitudes of 530 m and, after 7 h, 2,650 m. A hypoxia inhalation test (inspiratory oxygen fraction 0.15) was performed at low altitude in order to predict high-altitude hypoxaemia. Median Pa,O2 dropped from 9.8 kPa at low altitude to 7.0 kPa at high altitude. Mild exercise at a workload of 30 W further decreased Pa,O2. Two-thirds of all patients exhibited Pa,O2 of <6.6 kPa during exercise and, except for one patient, were asymptomatic. Patients were significantly less obstructed at an altitude of 2,650 m. Low forced expiratory volume in one second at baseline was associated with a low Pa,O2 at altitude. It is concluded that cystic fibrosis patients with baseline arterial oxygen tensions of >8.0 kPa safely tolerate an altitude of 2,650 m for several hours under resting conditions. The risk assessment of low in-flight oxygenation should encompass the whole clinical situation of cystic fibrosis patients, with special attention being paid to the presence of severe airway obstruction.

Adult↗
PubMed2006

The impact of altitude on early outcome following the Fontan operation.

BACKGROUND: The success of a Fontan circulation depends on several factors including low pulmonary vascular resistance. Pulmonary vascular resistance rises in response to hypoxia. Hypoxia is associated with altitude. Therefore, we wondered whether altitude is a risk factor for early failure after the Fontan operation. The aim was to test this hypothesis. METHODS: Data were obtained from all published series of 'total cavopulmonary' Fontan operations since 1990. The early failure rate from each series and the altitude of the respective cities were recorded. Early failure was defined as death, takedown of Fontan, or transplantation during the same hospital admission. The association between altitude and failure rate was investigated by rank correlation and logistic regression. RESULTS: 24 series were identified from centres situated at altitudes ranging from sea level to 520 metres. The plot of failure rate versus altitude suggests that failure rate increases with altitude. Logistic regression did not fit the data adequately. This was possibly due to the influence of unmeasured and unknown factors affecting the results, as well as the fact that centres were not randomly chosen but were self-selected by virtue of publishing their results. However, Spearman's rank correlation was 0.74 (p = 0.001). CONCLUSION: The early outcome of the Fontan circulation appears to be adversely affected by altitude.

Altitude↗
PubMed1999

The effect of moderate levels of simulated altitude on sustained cognitive performance.

Previous work has documented cognitive deficits at high altitudes (15,000-25,000 ft), but there is controversy for lower altitudes. This study looked at the effects of moderate altitudes--12,500 ft and 15,000 ft--on short-term memory in comparison to 2,000 ft. Seventy-two student pilots and instructors were first administered the Vocabulary, Digit Span, and Digit Symbol subtests from the Wechsler Adult Intelligence Scale-Revised, the Vandenberg Mental Rotation Test, and the near-contrast sensitivity portion of the Vistech VCTS 6000 chart. Participants then spent 1 1/2 hr at their designated altitude for cognitive testing. Participants performed a 30 min vigilance task while listening to an audiotape with instructions to recall radio calls prefaced by their assigned call sign. Half of the radio calls were high memory loads (at least 4 pieces of information), and half were low memory loads (no more than 2 pieces of information). No effects of altitude were found in performance on the Vigilance task. However, for readbacks of high memory load, significant deficits in recall were observed at 12,500 ft and 15,000 ft, whereas no effect of altitude was observed on recall of readbacks with low memory loads. These results indicate that, at altitude, short-term memory was exceeded for the readbacks requiring a larger amount of information to be recalled, and that cognitive deficits are found at lower altitudes than previously observed.

Adult↗
PubMed1993

Chronic obstructive pulmonary disease mortality. A role for altitude.

A map of US COPD mortality rates by state suggested that the relative hypoxia of increased altitude may be independently associated with COPD mortality. This was investigated using linear regression analysis of 1986 state-specific data on COPD mortality rates, history of cigarette consumption, and altitude. County seat altitudes and county populations were used to calculate the median altitude of state residents. We found independent significant associations between COPD and both smoking and altitude. State COPD mortality rose by 1/10(5) for every 5.4 increase in mean packs consumed per capita per year or for each 95-m increase in resident altitude. There was no association between altitude and smoking. If increased altitude does contribute to COPD mortality, persons with this disease may benefit from down-migration.

Altitude↗
PubMed2001

Current concept of chronic mountain sickness: pulmonary hypertension-related high-altitude heart disease.

High-altitude heart disease, a form of chronic mountain sickness, has been well established in both Tibet and Qinghai provinces of China, although little is known regarding this syndrome in other countries, particularly in the West. This review presents a general overview of high-altitude heart disease in China and briefly summarizes the existing data with regard to the prevalence, clinical features, and pathophysiology of the illness. The definition of high-altitude heart disease is right ventricular enlargement that develops primarily (by high-altitude exposure) to pulmonary hypertension without excessive polycythemia. The prevalence is higher in children than adults and in men than women, but is lower in both sexes of Tibetan high-altitude residents compared with acclimatized newcomers, such as Han Chinese. Clinical symptoms consist of headache, dyspnea, cough, irritability, and sleeplessness. Physical findings include a marked cyanosis, rapid heart and respiratory rates, edema of the face, liver enlargement, and rales. Most patients have complete recovery on descent to a lower altitude, but symptoms recur with a return to high altitude. Right ventricular enlargement, pulmonary hypertension, and remodeling of pulmonary arterioles are hallmarks of high-altitude heart disease. It is hoped that this information will assist in understanding this type of chronic mountain sickness, facilitate international exchange of data, and stimulate further research into this poorly understood condition.

Altitude Sickness↗
PubMed1993

Serum levels of adrenal androgens up to adrenarche in Peruvian children living at sea level and at high altitude.

Serum levels of adrenal androgens were measured in children of both sexes living at sea level and at high altitude using a cross-sectional design. The levels were compared in relation to age at each altitude (150 m and 3400 m above sea level), and the first significant increase in mean levels compared with values at preceding ages was assessed and defined as adrenarche. A total of 118 boys and 95 girls aged 6-12 years living at low altitude and 95 boys and 104 girls aged 7-15 years living at high altitude, all of them attending public schools, were studied. Serum dehydroepiandrosterone, dehydroepiandrosterone sulphate and androstenedione were measured by radioimmunoassay and height and weight by standard anthropometric techniques. There were two significant increases in serum levels of adrenal androgens, the first observed in children between 6 and 8 years at sea level, and between 7 and 9 years at high altitude, and the second in children between 10 and 12 years at sea level and between 12 and 15 years at high altitude. Serum adrenal androgen levels increased earlier in children at sea level than at high altitude. It is concluded that adrenarche occurs later at high altitude than at sea level.

Adrenal Cortex↗
PubMed2003

Simulated high altitude diving experiment for the underwater construction operation.

The simulated dive experiments were conducted at the high altitude of 4500 meters and 5000 meters, for the requirement of diving operation in the lakes at the altitude of 4442 meters for the construction of large-scale hydroelectric power station. The high & low pressure chamber-complex was used, and 15 professional divers participated in the experiment. The divers were stayed at the altitude of 4500 and 5000 meters for 7-9 days. Totally 85 persons-times of dives to the depths of 30-50 meters were operated; they stayed under the water for 30-90 minutes while processing physical activities. During the experiment, we studied the pressurization procedure, decompression table, and physiological functions of the divers. The results indicate that, although the relative pressure differences between the surface and underwater was larger at high altitude than at sea level, the appropriate prolongation of the compression time was able to prevent the difficulty in pressure regulation for the divers to avoid the injury of middle ear. Four tables of the decompression A, B, C and D was calculated with Haldane's theory, and the speed of decompression increased in the order from A to D. The safest procedure was C, and there was no decompression sickness and bubbles in body of the divers. The methods of decompression included underwater stage decompression, surface decompression, oxygen-breathing decompression, and repetitive diving decompression. The surface decompression was the most suitable method for the high altitude, as it could greatly decrease the time in the cold water for the divers. The power spectrum analysis of EEG (electroencephalogram) indicated that, when the divers were exposed to the altitude of 5000 meters, the delta activity in EEG increased, alpha and beta activity decreased. And the delta activity decreased, the alpha and beta activity increased while diving during a dry condition. According to the diving and decompression procedure studied under simulated conditions, 272 person-times of diving training and underwater operations were processed in a high altitude hydroelectric power station at the altitude of 4442 meters, including photographing, video-recording, measuring, and drilling. There were no signs and symptoms of decompression sickness and bubbles.

Adaptation, Physiological↗
PubMed2001

Current trends in altitude training.

Recently, endurance athletes have used several novel approaches and modalities for altitude training including: (i) normobaric hypoxia via nitrogen dilution (hypoxic apartment); (ii) supplemental oxygen; (iii) hypoxic sleeping devices; and (iv) intermittent hypoxic exposure (IHE). A normobaric hypoxic apartment simulates an altitude environment equivalent to approximately 2000 to 3000m (6560 to 9840ft). Athletes who use a hypoxic apartment typically 'live and sleep high' in the hypoxic apartment for 8 to 18 hours a day, but complete their training at sea level, or approximate sea level conditions. Several studies suggest that using a hypoxic apartment in this manner produces beneficial changes in serum erythropoietin (EPO) levels, reticulocyte count and red blood cell (RBC) mass, which in turn may lead to improvements in postaltitude endurance performance. However, other studies failed to demonstrate significant changes in haematological indices as a result of using a hypoxic apartment. These discrepancies may be caused by differences in methodology, the hypoxic stimulus that athletes were exposed to and/or the training status of the athletes. Supplemental oxygen is used to simulate either normoxic (sea level) or hyperoxic conditions during high-intensity workouts at altitude. This method is a modification of the 'high-low' strategy, since athletes live in a natural terrestrial altitude environment but train at 'sea level' with the aid of supplemental oxygen. Limited data regarding the efficacy of hyperoxic training suggests that high-intensity workouts at moderate altitude (1860m/6100ft) and endurance perfor- mance at sea level may be enhanced when supplemental oxygen training is utilised at altitude over a duration of several weeks. Hypoxic sleeping devices include the Colorado Altitude Training (CAT) Hatch (hypobaric chamber) and Hypoxico Tent System (normobaric hypoxic system), both of which are designed to allow athletes to sleep high and train low. These devices simulate altitudes up to approximately 4575 m/15006 ft and 4270 m/14005 ft, respectively. Currently, no studies have been published on the efficacy of these devices on RBC production, maximal oxygen uptake and/or performance in elite athletes. IHE is based on the assumption that brief exposures to hypoxia (1.5 to 2.0 hours) are sufficient to stimulate the release of EPO, and ultimately bring about an increase in RBC concentration. Athletes typically use IHE while at rest, or in conjunction with a training session. Data regarding the effect of IHE on haematological indices and athletic performance are minimal and inconclusive.

Acclimatization↗
PubMed1995

Effect of alcohol on acute ventilatory adaptation to mild hypoxia at moderate altitude.

OBJECTIVE: To evaluate the influence of alcohol on acute adaptation to mild hypoxia at moderate altitude. DESIGN: Randomized, double-blind, placebo-controlled crossover trial. SETTING: University clinic and mountaineering resort at altitudes of 171 m and 3000 m, respectively, in the Austrian Alps. PARTICIPANTS: 10 healthy male alpinists, 22 to 24 years of age. INTERVENTION: Single dose of 50 g of alcohol or placebo at altitudes of 171 m and 3000 m. MAIN OUTCOME MEASURES: Arterial oxygen pressure (Pao2) and arterial carbon dioxide pressure (Paco2) before and 1 hour after consumption of alcohol or placebo. RESULTS: At an altitude of 171 m, 50 g of alcohol caused no statistical change in Pao2 and Paco2 (median Pao2, 91.5 compared with 90.5 mm Hg [P = 0.89]; median Paco2, 37.5 compared with 36.0 mm Hg [P = 0.41]). At an altitude of 3000 m, the median Pao2 decreased from 69.0 to 64.0 mm Hg, a median decrease in the paired difference of 4.0 mm Hg (95.1% CI, 1.5 to 6.5 mm Hg; P < 0.01), and the median Paco2 increased from 32.5 to 34.0 mm Hg, a median increase in the paired difference of 3.0 mm Hg (95.1% CI, 2.0 to 4.0 mm Hg; P < 0.01) 1 hour after drinking 50 g of alcohol. Placebo did not influence Pao2 or Paco2 at either altitude. CONCLUSION: Alcohol inhibits the initial stages of adequate acute ventilatory adaptation to mild hypoxia at moderate altitude. Caution in the use of alcoholic beverages at moderate altitude is therefore necessary.

Adaptation, Physiological↗
PubMed1976

[Altitude adaptation. V. (conclusion). Morbidity and mortality. Literature].

The ability to adapt to extreme conditions is a continously working principle of man's evolution, in a permanent orientation to an optimal equilibrium between man and environment. A paradigm of biological adaptation is the condition of hypoxia at high altitudes, as one of the few environment constellations to which a pure biological and thus genetically based answer could be possible. The majority of adaptations are influenced by technological actions, which partially modify the environment in compensating unfavourable constellations (heating, clothing, housing, etc.). It is discussed, how far the adaptation to high altitudes produces transitory or permanent alterations with reference to constitution, perseverance, cold-sensitivity, diseases, duration of life, fertility, course of pregnancy, adaptations at the organ- and tissue-level, blood-composition, fluid-equilibrium of the body etc., which guarantee the survival of the individual and its successful reproduction with regard to the continuance of a mendel population. The elucidation of the question on genetic determination of features characteristic for high altitude inhabitants is difficult because we know next to nothing about the genetic determination of physiologic parameters. Studies on ethnic marker-genes (Ethiopia, South-America) give no reference to population differences. Remarkable is a striking prevalence of the blood-group O for all populations of high altitudes, but one must consider the effects of isolation in terms of the increase in the homozygote recessive alleles. We can propose, that in the primary settlement at high altitudes a "hard selection" was working, a kind of biological assortation-process from the beginning, which eliminated those individuals, who proved to be (for genetic reasons?) not adaptable. A good example for this are observations of cattle, from which 50% do not develop pulmonary hypertension when exposed to altitude, that means they already have a higher initial fitness. The non-adaptable animals have to be returned to the lowlands. In the F1-generation only 2% of the animals remaining at high altitude, develop "brisket disease". Possibly that means a sort of "out-mendeling" of "pulmonary-hypertension-genes", which may manifest themselves in the condition of hypoxia. Also the good adaptation of llamas is partially due to the fact that the camelids per se possess an outstanding O2 affinity and morphologically different red blood cells, which predispose this species to inhabit high altitudes. Parallel to considerations like these it could be imaginable, that e.g. the indianids of mongoloids in general, are genetically composed as fit to inhabit lowlands as well as highlands, in contrast to caucasoids and negroids. The largest mountain areas of the world (the Andes: 12 X 10(6)), the Himalayas 12 X 10(6)) are inhabited by populations of mongoloid ancestry, for about 10,000 years, a period, which ought to be long enough to make possible genetic specialisation, although it is not yet possible to prove it...

Acclimatization↗
PubMedDate not supplied

Effects of long-term high-altitude hypoxia on isolated fetal ovine coronary arteries.

OBJECTIVE: To examine the effects of long-term high-altitude hypoxia on the contractile properties of isolated fetal coronary arteries. METHODS: Maximal contractile responses (T(max)) to 90 mmol/L KCl and the thromboxane A(2) mimetic U46619 were measured in proximal (PLCx) and distal left circumflex (DLCx), left anterior descending (LAD), and right coronary arterial (RCA) rings from high-altitude and control fetuses. Paired studies were conducted with and without nitric oxide synthase (NOS) inhibitors, Nomega-nitro-L-arginine and Nomega-nitro-L-arginine ester. RESULTS: In high-altitude fetuses, 90 mmol/L KCl T(max) responses in both intact and NOS-blocked rings decreased by approximately 62% in PLCx, approximately 59% in DLCx, approximately 57% in LAD, and approximately 47% in RCA (n = 9-18/group; P <.05). High-altitude vessels also exhibited decreased sensitivity to U46619. NOS blockade potentiated T(max) to U46619 in the high-altitude RCA segments and augmented T(max) to U46619 in high-altitude RCA compared with its treated control counterpart (P <. 05). CONCLUSION: These results suggest that nitric oxide influences the pharmacologic responsiveness of the RCA to U46619. Furthermore, long-term high-altitude hypoxia significantly alters the contractile capabilities of fetal coronary arteries. These observations may partially explain the maintained redistribution of cardiac output to the fetal heart during exposure to long-term high-altitude hypoxia.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMedDate not supplied

Thrombosis as a complication of extended stay at high altitude.

BACKGROUND: There is limited knowledge about the medical problems of long term stay at high (> 3000 m) and extreme (> 5000 m) altitudes, as these areas are generally considered uninhabitable. METHODS: Prospectively collected clinical records of all patients hospitalized at Command Hospital, Western Command between November 1998 and February 2000 were reviewed to identify thrombotic complications among patients from high and extreme altitude areas as well as those from non-high altitude areas who were < 45 years of age. RESULTS: Of 20,257 hospital admissions during the study period, 1692 were from high and extreme altitude areas. Forty-six patients from these areas had thrombosis-related diseases compared to 17 from non-high altitude areas (odds ratio: 30.49; 95% CI: 17.06-51.67; p < 0.001). The mean (SD) age of all patients with thrombotic complications was 32 (8) years and all were men. The mean duration of stay at high and extreme altitudes of such patients was 10.2 (5.6) months. Only 25 were smokers (mean 5.2 pack-years) and 39 consumed alcohol (mean 54 ml/day). Apart from frostbite in 5, no other medical condition was noted in these patients. The vascular events were deep vein thrombosis (20), pulmonary thromboembolism (6), stroke (15), thrombosis of the abdominal veins (8), and retinal artery and peripheral arterial thrombosis (1 each). The presenting complaint in all patients with thrombosis of the abdominal veins was poorly localized pain in the upper abdomen followed by ascites (6/8). Five of these patients also had a large spontaneous splenic haematoma. None of the patients investigated was found to have a procoagulant disorder. CONCLUSION: Long term stay at high and extreme altitudes is associated with a 30 times higher risk of spontaneous vascular thrombosis. Veins are common sites of such thrombotic events. We also encountered thrombosis of the portal, splenic and superior mesenteric veins in our patients who had stayed at high and extreme altitudes.

Adult↗