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PubMed1982

Nitrous oxide analgesia and altitude.

The analgesic effectiveness of 50% nitrous oxide and oxygen or oxygen-enriched air, measured by variations in pain threshold, was studied at an altitude of 1460 m and simulated altitudes of sea level and 3300 m. At sea level pressures, 50% nitrous oxide exerted a similar analgesic effect to that found for morphine, raising the pain thresholds by a mean of 71.5%. At 1460 m, the increase in pain threshold produced was 40% and at 3300 m the increase in pain threshold was only 19%. The difference between the analgesic effects of nitrous oxide at each altitude was statistically significant. It is concluded that moderate altitudes significantly reduce the effectiveness of nitrous oxide in a manner directly related to the partial pressure of nitrous oxide at each altitude.

Adult↗
PubMed2006

High-altitude climate therapy reduces local airway inflammation and modulates lymphocyte activation.

High-altitude climate therapy is a well-established therapeutic option, which improves clinical symptoms in asthma. However, little is known about the underlying immunological mechanisms. The study investigates the influence of high-altitude climate therapy on airway inflammation and cellular components of specific and unspecific immune response. Exhaled NO significantly decreased within 3 weeks of therapy in patients with allergic and intrinsic, moderate and severe asthma. Interleukin-10 (IL-10)-secreting peripheral blood mononuclear cells (PBMC) increased within 3 weeks of therapy in six of 11 patients, whereas transforming growth factor-beta(1)-secreting PBMC remained stable. Furthermore, monocyte activation, assessed by CD80 expression significantly decreased during therapy. The frequency of CRTH2-expressing T cells decreased, while regulatory T cells (T(reg)) remained stable. FOXP3 and GATA-3 mRNA expression in CD4(+) T cells did not change, while interferon-gamma and IL-13 mRNA expression decreased in eight of 10 patients. The current data demonstrate that high-altitude climate therapy reduces local airway inflammation. Furthermore, monocytes switch towards a tolerogenic phenotype under high-altitude climate therapy. The T(reg)/Th2 ratio increases; however, because of the absence of antigens/allergens, no de novo differentiation of Th2 nor T(reg) cells is observed. The high-altitude climate therapy therefore may form the immunological basis for the endogenous control of allergen-driven diseases.

Adult↗
PubMed1996

Pain perception under chronic high-altitude hypoxia.

Following studies of respiratory sensory functions during high-altitude adaptation, pain perception investigations were carried out on European lowlanders during an expedition on the Bhrikuti peak, Himalaya (first ascent). Perception thresholds and discrimination performances of electrical stimuli applied to the skin were determined with a constant stimulus method. Additionally, Clark's Situational Pain Questionnaire was used to measure discriminability and response bias of the subjects' reports of pain. The tests were performed in the field under normoxic conditions, before and after ascent, and under hypoxic conditions at altitudes of 3500 and 5600 m. The tests were also performed in a control group under normoxic conditions and similar ambient temperatures. Under normoxic conditions, the expedition group differed from the control group and demonstrated a more stoic attitude and a lower pain threshold. At high altitudes, pain thresholds decreased through improved sensory discrimination performances. Hypoxia is supposed to be the main cause of this sensory adaptive reaction to altitude as psychological attitude remained unchanged and a decrease in ambient temperature was without effect on pain perception in the control group. Increased discrimination in pain perception may be a component of a general improvement in sensory processing during the early stages of altitude acclimatization.

Adult↗
PubMed2000

Influence of acute exposure to high altitude and hypoxemia on ventricular stimulation thresholds in pacemaker patients.

Cardiac stimulation threshold of implanted pacemakers may be influenced by a variety of endogenous and exogenous factors. High altitude provokes hypoxemia, which may change stimulation thresholds, besides causing other important physiological changes. The aim of our study was to investigate the influence of high altitude on ventricular stimulation thresholds in pacemaker patients. Thirteen patients (10 men; aged 65.5 +/- 4.8 years) with implanted single chamber pacemakers (nine with Pacesetter Regency SR+ with the Autocapture feature) were exposed to an altitude of 4,000 m above sea level, as simulated in a hypobaric chamber. Stepwise ascension was performed with a speed of 5 m/s starting at 450 m above sea level. A 5-minute rest was performed every 500 m to measure stimulation threshold at each step. After a stay of 30 minutes at 4,000 m stimulation threshold was measured, followed by a stepwise descent. Pacemaker interrogation and arterial blood gas analysis were performed at 450 and at 4,000 m, and a strength-duration curve was determined. Blood pressure, heart rate, and oxygen saturation were monitored continuously during the study. Ascent to 4,000 m above sea level induced a significant decrease in arterial pO2 (10.7 +/- 1.1 vs 5.5 +/- 0.3 kPa), pCO2 (5.3 +/- 0.3 vs 4.7 +/- 0.4 kPa), oxygen saturation measured by arterial blood gas analysis (95.5% +/- 1.2% vs 79.1% +/- 2.5%), and increase in pH (7.39 +/- 0.02 vs 7.45 +/- 0.04) (P < 0.0001). Stimulation thresholds and the strength-duration curve remained unchanged in all patients throughout the study. In conclusion, exposure to an altitude of 4,000 m above sea level with resultant hypobaric hypoxemia has no impact on ventricular stimulation thresholds. Therefore, in regard to the safety of pacing, pacemaker patients can safely be exposed to this altitude.

Acute Disease↗
PubMed1993

Time-dependently enhanced pressor responses in rat lungs after chronic exposure to high altitude.

To investigate the de-acclimatization process with respect to pulmonary vasoreactivity after high-altitude exposure, we performed a study of changes in pressor responses over time in salt-perfused lungs from rats that had been exposed to high altitude (HA, n = 41, 20 weeks at actual 2400 m). Comparisons were made with the lungs of rats kept at low altitude (n = 8, kept at 610 m). We studied HA rats from the time just after removal from high altitude to 2 weeks after the exposure. The pressor responses of HA lungs to both 0.5 microgram-angiotensin II and 5 min airway hypoxia (3% O2) just after the exposure did not differ from those of controls, but their responses began to increase within 12 h, and reached a maximum 3 days after exposure ended. The increase was time-dependent. We conclude that pulmonary vasopressor responses are enhanced time-dependently during the very early stages of de-acclimatization after high-altitude exposure.

Altitude↗
PubMed1995

Poor ventilatory response to mild hypoxia may inhibit acclimatization at moderate altitude in elderly patients after carotid surgery.

Peripheral chemoreceptors (carotid bodies) are the main sensing organs for hypoxaemia. During carotid surgery, the carotic body in the bifurcation of the common carotid artery is often involved and damaged or destroyed. Animals lose their ability to adapt to high altitude after experimental denervation of the carotid bodies. The objective of our study was to evaluate the ability of human patients to adapt to moderate altitude after single side carotid surgery. Blood gas analysis at rest at 171 m and after car and cable car transport to 1600 m before and after carotid surgery was performed. Mean(s.d.) paO2 decreased insignificantly from 74.8(3.56) at 171 m altitude to 71.6(2.07) at 1600 m (P = n.s.), means(s.d.) paCO2 decreased significantly from 36.2(2.86) to 31.4(2.7) mmHg (P < 0.05) before carotid surgery. Months after surgery, a significant drop in paO2 occurred after identical passive exposure to moderate altitude: mean(s.d.) paCO2 at 171 m 74.4(3.65) mmHg, at 1600 m 65.8(3.70) mmHg (P < 0.01), paCO2 did not change significantly. Mean(s.d.) paCO2 at 171 m: 36.0(2.35), at 1600 m 36.2(2.86) mmHg (P = n.s.). Although the sample investigated was small, after single side carotid surgery patients seem to lose their ability for satisfactory ventilatory response to acute exposure to moderate altitude. This is of possible alpine medical importance.

Acclimatization↗
PubMed1999

High-altitude illness induced by tooth root infection.

High-altitude illness may occur after recent pulmonary infection, but high-altitude illness after root canal therapy has not been described previously. A 44-year-old man is presented who skied to a 3333 m high peak in the Eastern Alps one day after he had undergone root canal therapy because of a tooth root infection. After 4 hours above 3000 m severe symptoms of high-altitude illness, including pulmonary oedema, developed. His condition improved after immediate descent. The next day he presented with local and general signs of infection which were successfully treated with gingival incisions and antibiotics. In conclusion, acute tooth root infection and root canal therapy may induce high-altitude illness at an altitude just above 3000 m.

Adult↗
PubMed2004

Pulmonary gas exchange at maximal exercise in Danish lowlanders during 8 wk of acclimatization to 4,100 m and in high-altitude Aymara natives.

We aimed to test effects of altitude acclimatization on pulmonary gas exchange at maximal exercise. Six lowlanders were studied at sea level, in acute hypoxia (AH), and after 2 and 8 wk of acclimatization to 4,100 m (2W and 8W) and compared with Aymara high-altitude natives residing at this altitude. As expected, alveolar Po2 was reduced during AH but increased gradually during acclimatization (61 +/- 0.7, 69 +/- 0.9, and 72 +/- 1.4 mmHg in AH, 2W, and 8W, respectively), reaching values significantly higher than in Aymaras (67 +/- 0.6 mmHg). Arterial Po2 (PaO2) also decreased during exercise in AH but increased significantly with acclimatization (51 +/- 1.1, 58 +/- 1.7, and 62 +/- 1.6 mmHg in AH, 2W, and 8W, respectively). PaO2 in lowlanders reached levels that were not different from those in high-altitude natives (66 +/- 1.2 mmHg). Arterial O2 saturation (SaO2) decreased during maximum exercise compared with rest in AH and after 2W and 8W: 73.3 +/- 1.4, 76.9 +/- 1.7, and 79.3 +/- 1.6%, respectively. After 8W, SaO2 in lowlanders was not significantly different from that in Aymaras (82.7 +/- 1%). An improved pulmonary gas exchange with acclimatization was evidenced by a decreased ventilatory equivalent of O2 after 8W: 59 +/- 4, 58 +/- 4, and 52 +/- 4 l x min x l O2(-1), respectively. The ventilatory equivalent of O2 reached levels not different from that of Aymaras (51 +/- 3 l x min x l O2(-1)). However, increases in exercise alveolar Po2 and PaO2 with acclimatization had no net effect on alveolar-arterial Po2 difference in lowlanders (10 +/- 1.3, 11 +/- 1.5, and 10 +/- 2.1 mmHg in AH, 2W, and 8W, respectively), which remained significantly higher than in Aymaras (1 +/- 1.4 mmHg). In conclusion, lowlanders substantially improve pulmonary gas exchange with acclimatization, but even acclimatization for 8 wk is insufficient to achieve levels reached by high-altitude natives.

Acclimatization↗
PubMed1997

High altitude-induced changes in alpha1-adrenergic receptors and Ins(1,4,5)P3 responses in cerebral arteries.

In response to high-altitude long-term hypoxemia, the cerebral arteries of fetal and adult sheep show decreased contractile responses to norepinephrine (NE) and other agonists. To test the hypothesis that hypoxia-induced developmental and vessel specific cerebral artery contractility changes are mediated, in part, by changes in alpha1-adrenergic receptor (alpha1-AR) density and/or NE-induced inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] responses, we performed the following study. In common carotid (Com) and main branch cerebral (MBC) arteries from normoxic adult ewes and near-term fetuses and those acclimatized to high altitude (3,820 m), we quantified alpha1-AR density (maximal binding in fmol/mg protein) and affinity (dissociation constant in nM) with the alpha1-AR antagonist [3H]prazosin. In addition, we quantified NE-induced Ins(1,4,5)P3 responses in these arteries. With long-term hypoxemia, alpha1-AR density in fetal and adult Com decreased 75% (from 113 +/- 18 to 28 +/- 5 fmol/mg protein) and 66% (from 54 +/- 3 to 18 +/- 4 fmol/mg protein), respectively, from normoxic control values. alpha1-AR density of the fetal and adult MBC decreased 76% (from 47 +/- 4 to 11 +/- 1 fmol/mg protein) and 61% (from 23 +/- 3 to 9 +/- 3 fmol/mg protein), respectively, from controls. In hypoxemic adult Com, the NE-induced Ins(1,4,5)P3 response decreased 51% (from 309 +/- 38 to 151 +/- 24%) from the control value. In fetal and adult MBC, long-term hypoxemia was associated with decreases of 35% (from 345 +/- 40 to 225 +/- 30%) and 44% (from 355 +/- 55 to 199 +/- 16%), respectively, from control values. We conclude that in the adult Com and MBC vessels, acclimatization to high-altitude, long-term hypoxemia was associated with significant decreases in both alpha1-AR density values and Ins(1,4,5)P3 responses to NE. Similarly, in the fetal MBC arteries, high-altitude hypoxemia was associated with marked attenuation of both alpha1-AR density and NE-induced Ins(1,4,5)P3 responses. The magnitude of decreases in NE-induced Ins(1,4,5)P3 responses in these vessels correlated fairly well with the decreases in alpha1-AR density. These findings suggest that changes in noradrenergic receptor-second messenger coupling may play a role in altered cerebrovascular tone in association with high-altitude acclimatization and other forms of long-term hypoxia in both fetus and adult.

Acclimatization↗
PubMed1997

Ins(1,4,5)P3 receptors in cerebral arteries: changes with development and high-altitude hypoxia.

We and others have shown that adrenergic-mediated contractile responses in cerebral vessels in vitro differ with vessel segment, with developmental age, and with high-altitude, long-term hypoxia. This is associated with significant differences in alpha 1-adrenergic receptor density and norepinephrine (NE)-induced response of the second messenger inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]. To test the hypothesis that vessel-specific, developmental, and hypoxic-associated contractility changes are mediated, in part, by changes in Ins(1,4,5)P3-receptor [Ins(1,4,5)P3-R] density or affinity, we performed the following study. In common carotid (Com), circle of Willis, and main branch anterior, middle, and posterior cerebral arteries (MBC) from normoxic fetal (approximately 140 days), newborn (3-5 days), and adult sheep and fetal and adult sheep acclimatized to high altitude, we quantified Ins(1,4,5)P3-R with [3H]Ins(1,4,5)P3. In normoxic Com, Ins(1,4,5)P3-R density values (fmol/mg protein) in fetus, newborn, and adult were 8 +/- 53, 150 +/- 18, and 357 +/- 21, respectively (P < 0.05). In normoxic MBC cerebral arteries, the receptor density values in the three age groups were 115 +/- 15, 105 +/- 9, 99 +/- 5 fmol/mg protein, respectively. For fetal and adult Com, high-altitude, long-term hypoxemia was associated with decreases in Ins(1,4,5)P3-R density of 32 (to 58 +/- 5) and 70% (to 109 +/- 12), respectively, from control values (P < 0.01). In MBC cerebral arteries of fetus and adult, hypoxic-associated decreases in Ins(1,4,5)P3-R density from control were 80 (to 23 +/- 3) and 47% (to 53 +/- 7), respectively (P < 0.01). Ins(1,4,5)P3 binding affinity to the receptor averaged 11.8 +/- 0.5 nM and did not vary significantly as a function of vessel type, developmental age, or hypoxia. In Com, but not in MBC, Ins(1,4,5)P3-R density increased dramatically with developmental age. This suggests that differences in Ins(1,4,5)P3-R density values may account, in part, for differences in contractile responses of the two artery types in the several age groups. In response to long-term, high-altitude hypoxia, Ins(1,4,5)P3-R density values in both fetal and adult Com and MBC decreased significantly, as did their NE-induced contraction. This suggests a cellular basis for changes in cerebrovascular contractility in response to long-term hypoxia and that Ins(1,4,5)P3-R may play a role in acclimatization responses to high altitude.

Aging↗
PubMed1997

Carotid baroreflex control of heart rate during acute exposure to simulated altitudes of 3,800 m and 4,300 m.

To examine the baroreflex response in humans during acute high-altitude exposure, the carotid baroreflex cardiac responsiveness was studied using a neck chamber in seven unacclimatized male subjects. Measurements were made in a high-altitude chamber on separate days at sea level and during 1-h exposure at two different altitudes of 3,800 m [partial pressure of oxygen in inspired air (PI(O2)) = 90 mmHg] and 4,300 m (PI(O2) = 82 mmHg). R-R intervals were plotted against neck chamber pressures, and the baroreceptor response was analyzed by applying a four-parameter sigmoidal logistic function. The baroreceptor response curve shifted downward in either altitude, reflecting a tachycardic response at high altitude, and the magnitude of the shift was greater at 4,300 m than at 3,800 m. There was no change in the sigmoidal parameters at 3,800 m compared with sea level except for a reduction (P < 0.05) of the minimum R-R interval. At 4,300 m the maximal R-R range, slope coefficient, minimum R-R interval, and maximal gain of the curve decreased significantly (P < 0.05) compared with sea level values, whereas the centering point of the curve remained unchanged. These results suggest that hypoxia (PI(O2) = 82 mmHg) reduces the sensitivity of carotid baroreflex cardiac response.

Adult↗
PubMed1975

Thermal responses of unclothed men exposed to both cold temperatures and high altitudes.

Six resting men were exposed to three temperatures (15.5, 21, 26.5 degrees C) for 120 min at three altitudes (sea level, 2,500 m, 5,000 m). A 60-min sea-level control at the scheduled temperature preceded the nine altitude episodes. Comparison of the base-line results at any one temperature showed no differences between rectal temperatures (Tre) or mean weighted skin temperatures (Tsk). After 120 min, Tre and Tsk not only depended on ambient temperature but also altitude. The initial rate of fall in Tre increased with altitude and equilibrium occurred earlier. At 15.5 degrees C, Tre was 0.3 degrees C lower at 5,000 m and 0.2 degrees C lower at 2,500 m than at sea level. Tsk was almost 2 degrees C higher at 15.5 degrees C at 5,000 m and 1 degrees C higher at 2,500 m than at sea level. Similar, smaller differences were observed at 21 degrees C. Mean weighted body temperature showed no change with altitude, but, since the gradient between core and shell was reduced, a shift of blood toward the periphery is implied.

Adolescent↗
PubMed1976

Alterations in the coronary circulation of man following ascent to 3,100 m altitude.

Alterations in coronary blood flow associated with adaptation to high altitude were examined. Three normal men native to low altitude were studied, first at sea level, and again after 10 days' sojourn at 3,100 m altitude. During rest at high altitude, a 32% decrease in coronary blood flow was largely offset by a 28% increase in coronary arterial O2 extraction to maintain myocardial O2 delivery. The increase in O2 extraction resulted mainly from a decrease in coronary sinus blood O2 content and saturation. However, coronary sinus O2 tension remained constant, implying a decrease in the affinity of hemoglobin for O2. These observations are consistent with the hypothesis that coronary blood flow is regulated to maintain constant myocardial tissue O2 tension (as reflected here by coronary sinus blood O2 tension). The absence of a decrease in coronary sinus O2 tension or a decrease in myocardial lactate extraction imply that myocardial hypoxia did not develop. Therefore, myocardial hypoxia is not the basis for the decrease in cardiac stroke volume at high altitude reported previously and also observed in the present study.

Adaptation, Physiological↗
PubMed1977

Effect of high-altitude exposure for 10 days on stroke volume and cardiac output.

Resting stroke volume and cardiac output of 50 normal healthy sea-level residents (group A) were estimated by the noninvasive technique of electrical impedance plethysmography. They were then airlifted to an altitude of 3,658 m and serial estimations carried out at 0-4 h and 5-8 h and on the 2nd, 3rd, 4th, 5th, and 10th days. The subjects were brought back to sea level and studied for up to 5 days. Thirty permanent residents of high altitude (group B) and sixteen lowlanders temporarily resident at high altitude (group C) were also subjected to similar studies. It was found that resting stroke volume and cardiac output of group A started falling immediately on arrival at high altitude, reached the minimum on the 3rd day and tended to improved on the 4th and 5th day, but showed a secondary fall on the 10th day. The reduction in stroke volume in this group was not fully compensated by tachycardia. On return to sea level the cardiac output normalized immediately, the stroke volume on the 2nd day. At sea level goup A had values similar to group B and at high altitude to group C.

Adult↗
PubMed1978

Urinary catecholamine excretion in temporary residents of high altitude.

Urinary catecholamine excretion was estimated in 50 lowlanders temporarily staying at altitudes above 3,000 m. They were divided in subgroups according to the length of their continuous stay. For comparison, 25 highlanders who were born and brought up at high altitude and 50 lowlanders who had never been to altitudes of more than 1,000 m were also studied. High catecholamine excretion was noted in temporary residents staying at high altitude for up to 30 days as compared to that in lowlanders (P greater than 0.01). The excretion rate gradually returned to basal values thereafter. Catecholamines were essentially similar in lowlanders and highlanders. The significance of these findings is discussed regarding the possible pathogenetic role of the sympathoadrenal system in the development of ill effects in respone to high-altitude exposure.

Adult↗
PubMed1980

Chronic propranolol treatment blunts right ventricular hypertrophy in rats at high altitude.

Chronic beta-receptor blockade has been reported to inhibit right ventricular hypertrophy in rats at high altitude. If so, we wanted to determine whether beta-receptor blockade or some other drug action were involved and whether the heart, the lung vessels, or blood alterations were affected. In rats, chronic treatment with DL-propranolol (2 mg/kg ip once daily) reduced right ventricular hypertrophy and polycythemia of chronic high altitude. D-Propranolol and metoprolol did not reduce hypoxia-induced right ventricular hypertrophy or polycythemia. In isolated lungs from low-altitude rats treated chronically with DL-propranolol or with D-propranolol the pressor response to acute hypoxia was blunted. Chronic DL-propranolol blunted the acute hypoxic pressor response and angiotensin II induced vasoconstriction in lungs from high-altitude rats. Two effects of DL-propranolol treatment were seen: 1) blockade of beta 2-adrenergic receptors, which reduced the right ventricular hypertrophy of high altitude through reduction of hematocrit; and 2) a non-beta-effect, which reduced vascular responsiveness to acute hypoxia in the isolated lung preparation.

Adaptation, Physiological↗
PubMed1981

Components of alveolar-arterial O2 gradient during rest and exercise at sea level and high altitude.

To determine the effects of exercise and high altitude on the contributions of shunt, ventilation-perfusion (V/Q) nonhomogeneity, and diffusion limitation to the alveolar-arterial O2 gradient (AaDo2), we measured pulmonary exchange of O2, CO2, and six inert gases (SF6, ethane, cyclopropane, halothane, diethyl ether, and acetone) during rest and exercise in unanesthetized dogs at sea level and after acute exposure to an altitude of 6,096 m in a hypobaric chamber. Shunt and dead-space fractions, calculated from inert gas measurements, did not change. High altitude decreased the inert gas partial pressure gradients between mixed alveolar gas and mixed end-capillary blood, indicating that V/Q relationships became more homogeneous. Exercise had no effect on these gradients. At sea level, AaDo2 was mainly due to V/Q nonhomogeneity, with a small portion due to shunt. At high altitude, the contribution of shunt became negligible and that of V/Q nonhomogeneity diminished. These improvements were partially offset, however, by a gradient due to diffusion limitation. Exercise had no effect on AaDo2 or any of its components. At high altitude, estimated pulmonary O2 diffusing capacity averaged 20.8 ml.min-1 at rest and 35.3 ml-min-1.Torr-1 during exercise.

Altitude↗
PubMed1981

Body fluid and hematologic changes in the toad exposed to 48 h of simulated high altitude.

Body fluid and hematologic changes were found in three groups of adult male toads that had been exposed to 48 h of continuous simulated altitudes of 12,000, 18,000, and 24,000 ft, respectively. Erythrocyte counts and hematocrit ratios were increased significantly in all the high-altitude-exposed animals compared with the control group of animals kept at sea level, whereas the hemoglobin concentrations were significantly increased only in the 18,000- and 24,000-ft-exposed animals. Exposure to high altitude generally caused a reduction of plasma volume, blood volume, extracellular fluid volume, and total body water. These reductions were markedly lower in the animals exposed to 24,000 ft. These simulated high-altitude effects on body fluids and hematology in the toad (Bufo melanostictus) were compared with those of the rat, birds, and humans acutely acutely exposed at various high altitudes and were found to be qualitatively similar.

Altitude↗