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PubMed1990

The sleep electrocardiogram at extreme altitudes (Operation Everest II)

To evaluate the effect of sleep at extreme altitudes upon heart rate and rhythm, continuous sleep monitoring was performed in 8 normal young men during a 40-day simulated ascent of Mt. Everest in a hypobaric chamber. Recordings were made for 1 hour before sleep, during sleep and for 1 hour after awakening in all subjects at 760 torr (sea level), in 7 subjects at 390 torr (5,490 m), in 6 at 347 torr (6,100 m) and in 4 at 282 torr (7,620 m). The following results were obtained: periods of sinus bradycardia occurred during sleep in all subjects at 3 altitudes with a mean heart rate of 41 +/- 0.5 beats/min compared to a rate of 44 +/- 2 beats/min at sea level; cycling of the heart rate, presumably due to periodic breathing, occurred in 14 of 17 studies at altitude but not at sea level (cycles consisted of bradycardia [40 beats/min] for 13 seconds and tachycardia [120 beats/min for 5 seconds]; and arrhythmias were observed in all subjects during sleep and consisted of transient bradycardia (heart rates as low as 20 beats/min), sinus pauses frequently associated with escape rhythms and occasional blocked P waves. No arrhythmias were observed at sea level. Simultaneous records of respiration and the electrocardiogram at 12,500 feet (3,810 m) in 5 other normal subjects revealed tachycardia occurring during hyperpnea and bradycardia occurring during apnea. Data indicate that during sleep in normal young subjects at high altitude, cycling of the heart rate with periodic breathing is common, as are bradyarrhythmias. The mechanism of these arrhythmias has yet to be defined.

Adult↗
PubMed1982

The pathophysiology of acute high-altitude illness.

Complex physiologic responses occur as nonacclimatized lowland dwellers ascend above 10,000 feet, with a resulting partial pressure of arterial oxygen of less than 60 mm Hg. There are marked hemodynamic changes and shifts in body fluids that may result in organ dysfunction. The suspected pathogenesis of these acute hypobaric hypoxic-induced illnesses is discussed. Cerebral dysfunction may present as acute mountain sickness or high-altitude cerebral edema. Usually asymptomatic high-altitude retinal hemorrhage and noncardiogenic high-altitude pulmonary edema also are described. All of these illnesses apparently represent a spectrum of pathologic states initiated by an exaggerated vascular response to hypoxia. With the exception of retinopathy, high-altitude illness can be prevented by slow ascent. Early recognition of cerebral or pulmonary edema and immediate descent will prevent serious consequences of nonacclimatized persons who are acutely exposed to hypobaric environments.

Acute Disease↗
PubMed1993

Effects of long-term, high-altitude hypoxemia on ovine fetal cardiac output and blood flow distribution.

OBJECTIVE: We sought to determine the effects of long-term hypoxemia on fetal cardiac output and flow distribution. STUDY DESIGN: We exposed six pregnant sheep to high altitude (3820 m) hypoxia from 30 to 135 days' gestation (term 146 days). Ten to 14 days after surgery we determined fetal cardiac output and organ blood flows by means of the radiolabeled microsphere technique during a baseline period and also during an additional 30-minute period of more severe added acute hypoxemia. RESULTS: Baseline maternal arterial PO2 was 60.7 +/- 1.7 torr and fell to 35.1 +/- 3.0 torr during the added acute hypoxemia. Fetal arterial PO2 decreased from 18.5 +/- 1.1 to 11.4 +/- 1.5 torr during added acute hypoxemia. Baseline fetal cardiac output was 351 +/- 55 ml/min/kg, which was significantly lower than previously reported values in low-altitude fetuses. Blood flow to critical organs such as the heart and brain was maintained at levels found in low-altitude fetuses, but flow to the carcass was significantly lower (-49%) than the mean value reported in the literature for low-altitude fetuses. Oxygen delivery was also maintained at normal levels to the brain and heart but was reduced in the kidneys (-31%), gastrointestinal tract (51%), and carcass (-58%). During added acute hypoxemia cardiac output did not change significantly; however, blood flow to the brain, heart, and adrenal glands increased 112%, 135%, and 156% (p < 0.05), respectively. CONCLUSION: We conclude that during long-term hypoxemia redistribution of fetal cardiac output is maintained favoring the brain and heart.

Adrenal Glands↗
PubMed1987

Evaluation of iron-deficiency anemia by an iron supplementation trial in children living at a 2,800-m altitude.

Hemoglobin, hematocrit, serum iron and total iron-binding capacity were measured in 38 apparently healthy children living in Quito (2:800 meters in altitude). One child was considered anemic according to the WHO reference adjusted to altitude (hemoglobin less than 12.3 g/dl) and 10 had transferrin saturation of less than 15%. Thirty children received orally 2 mg/kg per day of elemental iron for 3 mth. A significant increase in hemoglobin level, serum iron-concentration, and transferrin saturation, and a significant decrease in total iron-binding capacity were observed. Nine children increased their hemoglobin concentration by greater than 1 g/100 ml and could be considered as true anemics. At the end of the supplementation, only one child had a transferrin saturation coefficient of less than 15%. WHO references for hemoglobin adjusted to altitude seem to underestimate the prevalence of anemia for populations living at high altitudes.

Altitude↗
PubMed1996

High altitude and spontaneous preterm birth.

OBJECTIVE: To study the association between high altitude and spontaneous preterm birth. METHODS: Eleven placentas from cases of high altitude (3000 m) spontaneous preterm deliveries with no clinical predisposing cause were collected in Abha, a city of southern Saudi Arabia. The placentas were examined histologically using sections stained by periodic acid-Schiff and hematoxylin-eosin. The mean percentages of villi with syncytial knots and cytotrophoblastic cells were determined. RESULTS: Histology of the placenta samples showed an excessive formation of syncytial knots (45.4 +/- 13.3%) and cytotrophoblastic cells (52.7 +/- 15.2%) at terminal villi. CONCLUSION: The enhanced formation of syncytial knots and cytotrophoblastic cells is a histological feature of placental hypoxia, which may be secondary to maternal hypoxia resulting from high altitude hypoxia. Since placental hypoxia is associated with an increased incidence of spontaneous preterm birth, we suggest that high altitude may be involved in the etiology of spontaneous preterm birth.

Altitude↗
PubMed1993

Altitude and time of day effects on EEG spectral parameters.

Electroencephalographic (EEG) recordings were obtained from nine male subjects at sea level and again following rapid ascent to high altitude (4300 meters) at 0900, 1600, and 1830 h. Electroencephalographic data were subjected to Fast Fourier Transformation and analyzed for beta, spindle, alpha, theta, delta, and total amplitudes. Total amplitude increased from baseline to altitude while relative theta (absolute theta/total amplitude) decreased from baseline to altitude. Amplitude for absolute and relative spindle and total amplitude increased across the day. The results indicate that altitude exerts an effect on the waking electroencephalogram which can be quantified via spectral analysis.

Adult↗
PubMed1975

Cerebrospinal fluid alkalosis during high-altitude sojourn in unanesthetized ponies.

Unanesthetized adult female ponies were studied near sea level (250 m) and during sojourns to 3400 m (N=6) and 4300 m (N=7) altitude. The pH, PCO2, and PO2 of arterial blood and pH and PCO2 of cerebrospinal fluid (CSF) were measured under conditions of acute (1 hr) and chronic (1-45 days) hypoxia. Cerebrospinal fluid was sampled from the cisterna magna of the awake pony and arterial blood withdrawn from an indwelling arterial catheter. In both groups of animals, PaCO2 decreased slightly after 1 hr of hypoxia (delta PaCO2= - 0.6 mm Hg at 3400 m; - 3.9 mm Hg at 4300 m), decreased further after 1-5 days at high altitude (delta PaCO2= - 7.2 mm Hg at 3400 m; - 12.3 mm Hg at 4300 m) and then increased significantly after 6 days of chronic hypoxia (delta PaCO2= + 4.1 mm Hg at 3400 m; + 4.7 mm Hg at 4300 m). Although PaO2 decreased markedly during acute hypoxia, subsequent changes in PaCO2 at high altitude did not alter PaO2 from that observed during acute hypoxia (PaO2=52 mm Hg at 3400 m; 41 mm Hg at 4300 m). The pH of CSF increased during acute hypoxia (delta pH= + 0.013 unit at 3400 m; + 0.033 unit at 4300 m) and became more alkaline after 1-2 days at high altitude (delta pH= + 0.031 unit at 3400 m; + 0.064 unit at 4300 m). At 4300 m, CSF pH remained alkaline to control values throughout sojourn. Under these conditions of chronic hypocapnic hypoxia, CSF pH was imperfectly regulated and regulated in a magnitude equal to (3400 m) or less than (4300 m) arterial blood. Furthermore, the similarity of relative changes in CSF [HCO3-] and arterial [HCO3-] during chronic hypoxia may indicate a passive regulation of CSF [HCO3-] rather than local 'CSF-specific' mechanisms as previously proposed.

Acclimatization↗
PubMed1979

Acclimatization of newborn rats and guinea pigs to 3000 to 5000 m simulated altitudes.

Two species of newborn rodents (guinea pigs and rats) were acclimatized to simulated altitudes of 3000 to 6000 m during 2 to 8 weeks after birth. Body weight increase was significantly retarded in both species at altitudes of 5000 m and higher. Heart weight relative to body weight increased by 50% at 3000 m and 300% at 5000 m (after 7 weeks) in rats but was only 17% increased even at 5000 (6 weeks) in guinea pigs. Relative lung weights increased by 40% at 3000 m in rats and 5000 m in guinea pigs; at 5000 m rats showed a 130% increase. Hb-concentration increase (20%) was not significantly different in rats at 3000 m and 5000 m, respectively, in guinea pigs it was below 10% at 3000 m and around 40% at 5000 m. Half saturation pressures of blood (P50) increased in rats significantly compared to controls but not in guinea pigs. The results suggest that relative maturity and high blood oxygen affinity in newborn guinea pigs favor high altitude acclimatization. Immaturity of newborn rats, their low blood oxygen affinity and immature enzyme patterns are considered as reasons for the smaller resistance against high altitude stress compared to guinea pigs.

Acclimatization↗
PubMed1980

Pattern of breathing and mouth occlusion pressure during acclimatization to high altitude.

Pattern of breathing and mouth occlusion pressure have been investigated during a 6-day sojourn at an altitude of 3457 m in six resting subjects breathing ambient air or an hyperoxic mixture. It has been shown that ventilation increases and alveolar PCO2 decreases, both variables reaching a steady-state after about 4 days at altitude. Changes in ventilation are caused by modifications, at first, in the timing component of the respiratory cycle and later on, in the mean inspiratory airflow. This suggests that the output of the respiratory center is qualitatively modified during the acclimatization period. Mouth occlusion pressure, an index of neuromuscular inspiratory drive, increased on the first day at altitude, remaining constant thereafter. The mean inspiratory flow did not change on the first day, but progressively increased in the subsequent 3 days. The observation that flow increased in the face of a constant neuromuscular inspiratory drive suggests that during acclimatization to altitudes, the progressive increase in ventilation is due to changes in mechanics of the ventilatory pump rather than changes in central neural drive.

Acclimatization↗
PubMed1983

The contribution of central mechanisms rostral to the pons in high altitude ventilatory acclimatization.

In order to explore the role of suprapontine mechanisms in the ventilatory features of acclimatization to high altitude (HAVA) a study was made of: (a) normal cats after 48 h of exposure to a simulated altitude of 5500 m; (b) those same acclimatized cats 6 h following mid-collicular decerebration; (c) decerebrate cats after 48 h of exposure to a simulated altitude of 5500 m; (d) decerebrate cats after 48 h of exposure to room air at sea level. In a pilot study in which high altitude exposure was maintained for 30 days it was determined that normal cats show all of the manifestations of HAVA after 48 h. These were: increase of VI over acute hypoxic value and a maintained hyperventilation with normoxic inhaled gas; increase of both VT and f, the latter predominantly due to shortened TE; increase of VT/TI. Following decerebration the ventilatory pattern of these cats reverted to the preoperative, acute hypoxic exposure characteristics. Decerebrate cats maintained under normoxic conditions for 48 h showed no changes that were statistically significant, but brief (20 min) hypoxic tests indicated an increase of ventilatory response at the end of the second day. Decerebrate cats maintained for 48 h in the hypoxic environment showed all of the main features of HAVA. We conclude that suprapontine mechanisms in the intact cat exert a facilitatory influence which supports the development of HAVA, but if the structures in which those mechanisms normally reside are chronically removed, a comparable mechanism in the ponto-medullary region is capable of assuming the same function.

Acclimatization↗
PubMed1985

Gas diffusive conductance of sea-level hen eggs incubated at 2900 m altitude.

Sea level hen eggs, selected for their shell conductance (water vapor conductance, HH2O), were incubated at a simulated high altitude, PB = 529 Torr, ca. 2900 m, at 72% relative humidity (rh) to prevent excessive water loss due to hypobaric condition; they were transferred to 150 m 18-24 h before measurements. Control eggs were incubated at 150 m, PB = 750 Torr, rh = 60%. In 8- to 18-day embryos, total CO diffusive conductance, GCO; embyronic body mass, BM; oxygen consumption, MO2; blood hematocrit, Hct; hemoglobin concentration, [Hb]; and heart mass, HM, were measured. Total water loss was the same in both groups, 12% initial egg mass. However, the severe effects of high altitude: 72% mortality and 9% malformation, and reduced increases of BM and MO2, can be related partially to the strong hypocapnia, which resulted from the high shell conductance (GH2O = 18.1 mg X (d X Torr)-1, and was superimposed on the hypoxia. GCO was reduced, while Hct, [Hb] and HM were not significantly affected. When measurements were normalized to BM, MO2 and GCO were identical in the two groups, whereas [Hb] and HM were higher at 2900 m (differential growth). Thus, during incubation, gas diffusive conductance appeared to depend on embryo development and did not adapt to altitude hypoxia. Compared with controls, GCO in high-altitude eggs actually decreased in proportion to BM growth.

Altitude↗
PubMed1989

Muscle capillary tortuosity in high altitude mice depends on sarcomere length.

At given capillary-to-fiber ratio and sarcomere length, capillary tortuosity determines capillary length and the geometry of blood-tissue exchange in muscles. It is therefore an important determinant of the potential efficiency of O2 supply to the muscle fibers. Reports have indicated that capillary tortuosity increases with adaptation to hypoxia. Unfortunately, sarcomere length was not taken into account. Because capillary tortuosity increases substantially as the muscle shortens, it is important to measure sarcomere length when comparing capillary configuration among muscles. We addressed the question of whether or not capillary tortuosity is greater in skeletal muscles of high altitude mice compared to sea-level, when account is taken of sarcomere length. Calf and thigh muscles of high altitude (3800 m; inspired PO2, 91 mm Hg) and sea-level deer mice, Peromyscus maniculatus, were perfusion-fixed in situ at sarcomere lengths ranging from 1.9 to 2.4 microns. Capillary-to-fiber ratio, capillary length per volume of fiber, and the degree of orientation (anisotropy) of capillaries were estimated by morphometry. In both sea-level and high altitude mice, capillaries were relatively straight in extended muscles, and substantially more tortuous in muscles fixed at shorter sarcomere length. There was no systematic difference in the degree of tortuosity of capillaries in the high altitude compared to sea-level mice, when account was taken of sarcomere length. Capillary length per volume of muscle fiber and capillary-to-fiber ratio were not significantly different between the two groups.

Adaptation, Physiological↗
PubMed1992

CO2 and avian eggshell formation at high altitude.

We tested the hypothesis that altitude-induced hypocapnia in hens reduces eggshell conductance to water vapor (GH2O). Seven laying hens (Gallus domesticus) native to 1200 m were chronically exposed to high altitude (3800 m), and then to high altitude with sufficient inspired CO2 to relieve hypocapnia (3800 m + CO2). Egg GH2O was measured gravimetrically, shell thickness was measured with a micrometer, and aggregate pore area was calculated from measured values using Fick's law. Comparing results at 1200 m (n = 118) and 3800 m (n = 102), GH2O was reduced from 13.9 +/- 0.2 to 12.6 +/- 0.2 mg/(d.Torr)(mean +/- SE), shell thickness was reduced from 0.297 +/- 0.003 mm to 0.287 +/- 0.003 mm, and calculated aggregate pore area per egg was reduced from 1.97 +/- 0.03 mm2 to 1.72 +/- 0.03 mm2. When hypocapnia was relieved at 3800 m + CO2 (n = 82), GH2O was reduced even further to 11.1 +/- 0.2 mg/(d.Torr), shell thickness increased to 0.305 +/- 0.003 mm, and aggregate pore area was reduced to 1.61 +/- 0.03 mm2. Based on these results we reject our hypothesis. We conclude that hypocapnia is responsible for thin eggshells at altitude. Other physiological stimuli must cause the reductions in eggshell GH2O and pore area.

Altitude↗
PubMed1995

Possible role of dopamine in ventilatory acclimatization to high altitude.

Ventilatory acclimatization to high altitude is accompanied by increased hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses which may reflect increased carotid body chemosensitivity. Dopamine is an inhibitory neuromodulator of the carotid body and its activity may be reduced by hypoxic exposure. To determine whether decreased dopaminergic activity could account for the increased chemosensitivity of acclimatization, we examined the response to peripheral dopamine receptor (D2) blockade with domperidone on HVR and HCVR in awake cats before and after exposure to simulated altitude of 14,000 ft for 2 days. During anesthesia, we also examined the effects of domperidone on carotid body responses to hypoxia and hypercapnia in acclimatized and low altitude cats. Two days' exposure to hypobaric hypoxia produced an increase in HVR and HCVR. Before acclimatization, domperidone augmented HVR and HCVR, but there was no effect after acclimatization. In anesthetized low altitude cats, domperidone increased carotid body responses to hypoxia and hypercapnia, but had no effect in acclimatized cats. These results indicate that decreased endogenous dopaminergic activity may contribute to increased ventilatory and chemoreceptor responsiveness to hypoxia and hypercapnia during hypoxic ventilatory acclimatization.

Acclimatization↗
PubMed1996

Fiber capillarization in flight muscle of pigeons native and flying at altitude.

We examined structural characteristics for fiber O2 supply in the highly aerobic flight muscle of 5 pigeons (Columbia livia; body mass 223--317 g) native and actively flying at altitude (La Paz, Bolivia; 3750 m). Whereas deep sites were significantly more aerobic and highly vascularized than superficial in altitude (A) but not sea-level (SL) group, both sites showed a number of similarities between the two groups. The cross-sectional area of aerobic fibers (> or = 90% of fiber number) linearly increased with body mass (r 0.84; P < 0.0005) but was not smaller in A for their body mass, and there was no reduction in the size of glycolytic fibers compared to SL. The relationships between fiber capillarization and the sectional area of aerobic fibers in transverse sections or mitochondrial volume density were not altered in A compared to SL. The results indicate that the factors which determine the relationships between fiber capillarization and ultrastructure in the muscles were not altered by the adaptation to altitude. Differences between samples were related to the relative sectional area of aerobic fibers and mitochondrial volume density, not the chronic exposure to altitude.

Altitude↗
PubMed1992

Metabolic adaptation of myocardial mitochondria to mild altitude hypoxia.

We studied the metabolic parameters of myocardial mitochondria (respiration, respiratory control index, oxidative phosphorylation rapidity and coefficient of oxidative phosphorylation) in two groups of rats: one living at an altitude of 140 m above sea level (control group) and the other living from birth at an altitude of 1350 m above sea level for 2 and 4 months (experimental group). Compared with the control rats, the experimental rats during 2 and 4 months of mild altitude acclimatization increased their basal and stimulated respiration, as well as the rapidity of energy production by myocardial mitochondria. The coefficient of oxidative phosphorylation under mild altitude hypoxia decreased but the respiratory control index did not change. We explain these alterations of heart muscle metabolism at the mitochondrial level as an adaptation to the mild hypoxic conditions.

Altitude↗
PubMed1994

Role of oxygen free radicals in altitude-related disorders.

A massive expansion of mountain tourism and the practice of sports at altitude (mountaineering, skiing, cycling, hang-gliding, parapente, etc) has been observed in the last decades. This emphasis on new forms of sports and recreation represented as a social phenomenon is accompanied by an increase in the mountain associated-disorders and related-accidents. These include headache, lassitude, pain, difficulty in breathing, rapid heartbeat, and in the worst of the cases loss of consciousness, always possible, manifest by poor judgement, fatigue, etc, and death. However, medical studies are rare, mainly because the molecular mechanisms of tissue damage induced by oxygen free radicals are still poorly understood. Therefore, the goals of the present report are: 1) to summarize the main adaptations of the body at high altitude, introducing the concepts of altitude sickness and oxygen free radicals and their relation; 2) to propose a mechanism of action of oxygen free radicals in the development of this pathology, with special attention in hypoxia and related mechanisms; 3) to suggest a role for antioxidants in the therapy of altitude-related disorders.

Acclimatization↗
PubMed2006

Antibody responses to Plasmodium falciparum vaccine candidate antigens in three areas distinct with respect to altitude.

Antibody levels against malaria antigens were measured among patients presenting with uncomplicated malaria at health centers from three locations in Zimbabwe (Bindura, Chiredzi and Kariba) that are distinct with regard to altitude and climatic conditions. Antibody levels were determined by ELISA using the antigens, apical membrane antigen 1 (AMA-1), erythrocyte binding antigen 175 (EBA-175), circumsporozoite surface protein (CSP), merozoite surface protein 1 (MSP-1) and Pfg27. For all the antigens tested, IgG and IgM levels were higher for Bindura (altitude 1100 m) compared to Kariba (<600 m, altitude) and Chiredzi (approximately 600 m, altitude) with the exception of IgG and IgM to AMA-1 and EBA-175 which were similar between Chiredzi and Bindura. Plasma samples were further analyzed for their functional activity by testing their ability to inhibit the growth of Plasmodium falciparum in culture. Our results, determined by microscopy and verified by the LDH assay revealed that plasma from the three locations had similar inhibitory activity against the growth of P. falciparum in vitro. Our data revealed that highest growth inhibition correlated with the highest levels of MSP-1 antibody values.

Adolescent↗