Alkaline shift in lumbar and intracranial CSF in man after 5 days at high altitude

1976 ◽  
Vol 41 (1) ◽  
pp. 93-97 ◽  
Author(s):  
R. B. Weiskopf ◽  
R. A. Gabel ◽  
V. Fencl
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
High Altitude ◽  
Sea Level ◽  
Jugular Bulb ◽  
Alveolar Ventilation ◽  
Simulated Altitude ◽  
Healthy Male ◽  
Alkaline Shift ◽  
Breathing Room

In six healthy male volunteers at sea level (PB 747–759 Torr), we measured pH and PCO2 in cerebrospinal fluid (CSF), and in arterial and jugular bulb blood; from these data we estimated PCO2 (12) and pH for the intracranial portion of CSF. The measurements were repeated after 5 days in a hypobaric chamber (PB 447 Torr). Both lumbar and intracranial CSF were significantly more alkaline at simulated altitude than at sea level. Decrease in[HCO3-] IN lumbar CSF at altitude was similar to that in blood plasma. Bothat sea level and at high altitude, PCO2 measured in the lumbar CSF was higher than that estimated for the intracranial CSF. At altitude, hyperoxia, incomparison with breathing room air, resulted in an increase in intracranialPCO2, and a decrease in the estimated pH in intracranial CSF. With hyperoxia at altitude, alveolar ventilation was significantly higher than during sea-level hyperoxia or normoxia, confirming that a degree of acclimatization hadoccurred. Changes in cerebral arteriovenous differences in CO2, measuredinthree subjects, suggest that cerebral blood flow may have been elevated after 5 days at altitude.

Composition of cerebral fluids in goats adapted to high altitude

1979 ◽  
Vol 47 (3) ◽  
pp. 508-513 ◽  
Author(s):  
V. Fencl ◽  
R. A. Gabel ◽  
D. Wolfe
Keyword(s):  
Cerebrospinal Fluid ◽  
High Altitude ◽  
Sea Level ◽  
Interstitial Fluid ◽  
Ionic Composition ◽  
Central Chemoreceptors ◽  
Alkaline Shift ◽  
Artificial Cerebrospinal Fluid ◽  
Simulated High Altitude

We explored the ionic composition of cerebral interstitial fluid (cISF) in six unanesthetized goats at sea level (SL) and again after 5 days at a simulated high altitude (HA) of 4,300 m. By measuring net transependymal fluxes of HCO3-, Cl-, and lactate during ventriculocisternal perfusions with lactate-free artificial cerebrospinal fluid (CSF) with various [HCO3-] and [Cl-], we determined [HCO3-] and [Cl-] in the inflowing perfusate that produced zero flux, which are estimates of the concentrations of these ions in cISF. Ventilatory acclimatization to HA was established in the goats with alkaline shift in cisternal CSF pH. At SL zero flux of HCO3- and of Cl- occurred when [HCO3-] and [Cl-] in the perfusate were equal to those in CSF. At HA Cl- flux again was zero when [Cl-] in perfusate and in the goat's own CSF were equal; however, for HCO3-, zero flux occurred at HA when [HCO3-] in perfusate was significantly lower than in CSF. Mean transependymal washout of lactate was 16 times larger at HA than at SL. We conclude that at SL [HCO3-] and [Cl-] in CSF were the same as in cISF. In goats adapted to HA [Cl-] in cISF and in CSF were again equal, whereas [HCO3-] in cISF was lower and [lactate] presumably higher than in CSF. The fluid surrounding the central chemoreceptors appears to be more acidic in goats acclimatized to HA than at SL despite the alkalosis in cisternal CSF. This may contribute to ventilatory acclimatization to HA.

Effect of peripheral chemoreceptor denervation on acclimatization of goats during hypoxia

1981 ◽  
Vol 50 (2) ◽  
pp. 392-398 ◽  
Author(s):  
H. V. Forster ◽  
G. E. Bisgard ◽  
J. P. Klein
Keyword(s):  
Sea Level ◽  
Chronic Hypoxia ◽  
Alveolar Ventilation ◽  
Simulated Altitude ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Carotid Chemoreceptors ◽  
Co2 Output

The purpose of this study was to determine the effect of peripheral chemoreceptor denervation on ventilatory acclimatization of goats during chronic hypoxia. After 1 h of stimulated altitude (PB 450 Torr), arterial O2 tension (PaO2) in seven normal goats averaged 42 Torr, and arterial CO2 tension (PaCO2) was 1.3 Torr below control (P less than 0.001). In these goats nearly 66% of the increase in alveolar ventilation (VA) associated with acclimatization occurred between 1.5 and 4 h of hypoxia. Acclimatization was complete by the 3rd day of hypoxia, and it caused 1) a 23% increase in VA/CO2 output (P less than 0.001); 2) a 5-Torr increase in PaO2 (P less than 0.001); and 3) a 6.5-Torr decrease in PaCO2 (P less than 0.001). Denervation of the carotid chemoreceptors in seven goats caused hypoventilation during eupnea at sea level (PaCO2 change from control +7 Torr, P less than 0.001). Denervation also attenuated but did not eliminate peripheral chemoreceptor responsiveness. No additional changes were observed following attempted denervation of the aortic chemoreceptors. After 1 h of simulated altitude (PB 530 Torr), PaO2 in the denervated goats averaged 46 Torr, and PaCO2 was increased 1.1 Torr above control (P less than 0.001). In these goats VA did not change significantly during the subsequent 3 days of hypoxia. Accordingly, we conclude that the peripheral chemoreceptors are essential for ventilatory acclimatization of goats during chronic hypoxia.

Cerebrospinal fluid in man native to high altitude

1964 ◽  
Vol 19 (2) ◽  
pp. 319-321 ◽  
Author(s):  
J. W. Severinghaus ◽  
A. Carceleń B.
Keyword(s):  
Cerebrospinal Fluid ◽  
High Altitude ◽  
Sea Level ◽  
Regulation Of Respiration ◽  
Acid Base ◽  
Peripheral Chemoreceptor ◽  
Arterial Blood ◽  
Blood Ph ◽  
The Difference

CSF pH was shown in a prior report to remain essentially constant during 8 days of acclimatization to 3,800 m. In order to further evaluate the possible role of CSF acid-base equilibria in the regulation of respiration, 20 Peruvian Andean natives were studied at altitudes of 3,720–4,820 m. In ten subjects at 3,720 m, means were: CSF pH 7.327, Pco2 43, HCO3- 21.5, Na+ 136, K+ 2.6, Cl- 124, lactate 30 mg/100 ml. Arterial blood: pH 7.43, Pco2 32.5, HCO3- 21.3, Na+ 136, K+ 4.2, Cl- 107, hematocrit 49, SaOO2 89.6. In six subjects at 4,545 m and four at 4,820 m CSF values were not significantly different; mean arterial Pco2 was 32.6 and 32.3, respectively. The only significant variations with altitude were the expected lowering of PaOO2 to 47 and 43.5 mm Hg, and of SaOO2 to 84.2 and 80.7, and increase of hematocrit to 67% and 75%, respectively. The natives differed from recently acclimatized sea-level residents in showing less ventilation (higher Pco2) in response to the existing hypoxia, and less alkaline arterial blood. The difference appears to relate to peripheral chemoreceptor response to hypoxia rather than central medullary chemoreceptor. respiratory regulation at high altitude; chronic acclimatization to altitude; peripheral chemoreceptor response to hypoxia; CSF and medullary respiratory chemoreceptors Submitted on June 12, 1963

scholarly journals Global REACH 2018: renal oxygen delivery is maintained during early acclimatization to 4,330 m

2020 ◽  
Vol 319 (6) ◽  
pp. F1081-F1089
Author(s):  
Andrew R. Steele ◽  
Michael M. Tymko ◽  
Victoria L. Meah ◽  
Lydia L. Simpson ◽  
Christopher Gasho ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
High Altitude ◽  
Renal Blood Flow ◽  
Sea Level ◽  
Oxygen Delivery ◽  
Acid Base ◽  
Altitude Acclimatization ◽  
High Altitude Acclimatization ◽  
Renal Oxygen

Early acclimatization to high altitude is characterized by various respiratory, hematological, and cardiovascular adaptations that serve to restore oxygen delivery to tissue. However, less is understood about renal function and the role of renal oxygen delivery (RDO2) during high altitude acclimatization. We hypothesized that 1) RDO2 would be reduced after 12 h of high altitude exposure (high altitude day 1) but restored to sea level values after 1 wk (high altitude day 7) and 2) RDO2 would be associated with renal reactivity, an index of acid-base compensation at high altitude. Twenty-four healthy lowlander participants were tested at sea level (344 m, Kelowna, BC, Canada) and on day 1 and day 7 at high altitude (4,330 m, Cerro de Pasco, Peru). Cardiac output, renal blood flow, and arterial and venous blood sampling for renin-angiotensin-aldosterone system hormones and NH2-terminal pro-B-type natriuretic peptides were collected at each time point. Renal reactivity was calculated as follows: (Δarterial bicarbonate)/(Δarterial Pco2) between sea level and high altitude day 1 and sea level and high altitude day 7. The main findings were that 1) RDO2 was initially decreased at high altitude compared with sea level (ΔRDO2: −22 ± 17%, P < 0.001) but was restored to sea level values on high altitude day 7 (ΔRDO2: −6 ± 14%, P = 0.36). The observed improvements in RDO2 resulted from both changes in renal blood flow (Δ from high altitude day 1: +12 ± 11%, P = 0.008) and arterial oxygen content (Δ from high altitude day 1: +44.8 ± 17.7%, P = 0.006) and 2) renal reactivity was positively correlated with RDO2 on high altitude day 7 ( r = 0.70, P < 0.001) but not high altitude day 1 ( r = 0.26, P = 0.29). These findings characterize the temporal responses of renal function during early high altitude acclimatization and the influence of RDO2 in the regulation of acid-base balance.

Cardiovascular autonomic modulation and activity of carotid baroreceptors at altitude

1998 ◽  
Vol 95 (5) ◽  
pp. 565-573 ◽  
Author(s):  
Luciano BERNARDI ◽  
Claudio PASSINO ◽  
Giammario SPADACINI ◽  
Alessandro CALCIATI ◽  
Robert ROBERGS ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
High Altitude ◽  
Sea Level ◽  
Skin Blood Flow ◽  
Low Frequency ◽  
Sympathetic Activation ◽  
High Altitude Natives

1.To assess the effects of acute exposure to high altitude on baroreceptor function in man we evaluated the effects of baroreceptor activation on R–R interval and blood pressure control at high altitude. We measured the low-frequency (LF) and high-frequency (HF) components in R–R, non-invasive blood pressure and skin blood flow, and the effect of baroreceptor modulation by 0.1-Hz sinusoidal neck suction. Ten healthy sea-level natives and three high-altitude native, long-term sea-level residents were evaluated at sea level, upon arrival at 4970 ;m and 1 week later. 2.Compared with sea level, acute high altitude decreased R–R and increased blood pressure in all subjects [sea-level natives: R–R from 1002±45 to 775±57 ;ms, systolic blood pressure from 130±3 to 150±8 ;mmHg; high-altitude natives: R–R from 809±116 to 749±47 ;ms, systolic blood pressure from 110±12 to 125±11 ;mmHg (P< 0.05 for all)]. One week later systolic blood pressure was similar to values at sea level in all subjects, whereas R–R remained elevated in sea-level natives. The low-frequency power in R–R and systolic blood pressure increased in sea-level natives [R–R-LF from 47±8 to 65±10% (P< 0.05), systolic blood pressure-LF from 1.7±0.3 to 2.6±0.4 ln-mmHg2 (P< 0.05)], but not in high-altitude natives (R–R-LF from 32±13 to 38±19%, systolic blood pressure-LF from 1.9±0.5 to 1.7±0.8 ln-mmHg2). The R–R-HF decreased in sea-level natives but not in high-altitude natives, and no changes occurred in systolic blood pressure-HF. These changes remained evident 1 week later. Skin blood flow variability and its spectral components decreased markedly at high altitude in sea-level natives but showed no changes in high-altitude natives. Neck suction significantly increased the R–R- and systolic blood pressure-LF in all subjects at both sea level and high altitude. 3.High altitude induces sympathetic activation in sea-level natives which is partially counteracted by active baroreflex. Despite long-term acclimatization at sea level, high-altitude natives also maintain active baroreflex at high altitude but with lower sympathetic activation, indicating a persisting high-altitude adaptation which may be genetic or due to baroreflex activity not completely lost by at least 1 year's sea-level residence.

scholarly journals Adenosine receptor-dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans

2017 ◽  
Vol 122 (4) ◽  
pp. 795-808 ◽  
Author(s):  
Ryan L. Hoiland ◽  
Anthony R. Bain ◽  
Michael M. Tymko ◽  
Mathew G. Rieger ◽  
Connor A. Howe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Adenosine Receptor ◽  
Hypobaric Hypoxia ◽  
End Tidal ◽  
Double Blinded

Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, and placebo-controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]), ventilation (pneumotachography), blood pressure (finger photoplethysmography), heart rate (electrocardiogram), CBF (duplex ultrasound), and intracranial blood velocities (transcranial Doppler ultrasound) were measured during 5-min stages of isocapnic hypoxia at sea level (98, 90, 80, and 70% [Formula: see text]). Ventilation, [Formula: see text] and [Formula: see text], blood pressure, heart rate, and CBF were also measured upon exposure (128 ± 31 min following arrival) to high altitude (3,800 m) and 6 h following theophylline administration. At sea level, although the CBF response to hypoxia was unaltered pre- and postplacebo, it was reduced following theophylline ( P < 0.01), a finding explained by a lower [Formula: see text] ( P < 0.01). Upon mathematical correction for [Formula: see text], the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e., response slope) was not different between trials, irrespective of [Formula: see text]. At high altitude, theophylline ( n = 6) had no effect on CBF compared with placebo ( n = 6) when end-tidal gases were comparable ( P > 0.05). We conclude that adenosine receptor-dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans. NEW & NOTEWORTHY The signaling pathways that regulate human cerebral blood flow in hypoxia remain poorly understood. Using a randomized, double-blinded, and placebo-controlled study design, we determined that adenosine receptor-dependent signaling is not obligatory for the regulation of human cerebral blood flow at sea level; these findings also extend to high altitude.

Ischemic preconditioning does not improve peak exercise capacity at sea level or simulated high altitude in trained male cyclists

2015 ◽  
Vol 40 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Elizabeth A. Hittinger ◽  
Jennifer L. Maher ◽  
Mark S. Nash ◽  
Arlette C. Perry ◽  
Joseph F. Signorile ◽  
...  
Keyword(s):  
Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Exercise Capacity ◽  
Ischemic Preconditioning ◽  
Oxygen Delivery ◽  
Peak Exercise ◽  
Arterial Hypoxemia ◽  
Cardiovascular Hemodynamics ◽  
Simulated High Altitude

Ischemic preconditioning (IPC) may improve blood flow and oxygen delivery to tissues, including skeletal muscle, and has the potential to improve intense aerobic exercise performance, especially that which results in arterial hypoxemia. The aim of the study was to determine the effects of IPC of the legs on peak exercise capacity (Wpeak), submaximal and peak cardiovascular hemodynamics, and peripheral capillary oxygen saturation (SpO2) in trained males at sea level (SL) and simulated high altitude (HA; 13.3% FIO2, ∼3650 m). Fifteen highly trained male cyclists and triathletes completed 2 Wpeak tests (SL and HA) and 4 experimental exercise trials (10 min at 55% altitude-specific Wpeak then increasing by 30 W every 2 min until exhaustion) with and without IPC. HA resulted in significant arterial hypoxemia during exercise compared with SL (73% ± 6% vs. 93% ± 4% SpO2, p < 0.001) that was associated with 21% lower Wpeak values. IPC did not significantly improve Wpeak at SL or HA. Additionally, IPC failed to improve cardiovascular hemodynamics or SpO2 during submaximal exercise or at Wpeak. In conclusion, IPC performed 45 min prior to exercise does not improve Wpeak or systemic oxygen delivery during submaximal or peak exercise at SL or HA. Future studies must examine the influence of IPC on local factors, such as working limb blood flow, oxygen delivery, and arteriovenous oxygen difference as well as whether the effectiveness of IPC is altered by the volume of muscle made ischemic, the timing prior to exercise, and high altitude acclimatization.

Ventilation-perfusion inequality in normal humans during exercise at sea level and simulated altitude

1985 ◽  
Vol 58 (3) ◽  
pp. 978-988 ◽  
Author(s):  
G. E. Gale ◽  
J. R. Torre-Bueno ◽  
R. E. Moon ◽  
H. A. Saltzman ◽  
P. D. Wagner
Keyword(s):  
Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Statistical Significance ◽  
Barometric Pressure ◽  
Bicycle Ergometer ◽  
Lung Model ◽  
Inert Gas ◽  
Topographical Distribution ◽  
Normal Humans

To investigate the effects of both exercise and acute exposure to high altitude on ventilation-perfusion (VA/Q) relationships in the lungs, nine young men were studied at rest and at up to three different levels of exercise on a bicycle ergometer. Altitude was simulated in a hypobaric chamber with measurements made at sea level (mean barometric pressure = 755 Torr) and at simulated altitudes of 5,000 (632 Torr), 10,000 (523 Torr), and 15,000 ft (429 Torr). VA/Q distributions were estimated using the multiple inert gas elimination technique. Dispersion of the distributions of blood flow and ventilation were evaluated by both loge standard deviations (derived from the VA/Q 50-compartment lung model) and three new indices of dispersion that are derived directly from inert gas data. Both methods indicated a broadening of the distributions of blood flow and ventilation with increasing exercise at sea level, but the trend was of borderline statistical significance. There was no change in the resting distributions with altitude. However, with exercise at high altitude (10,000 and 15,000 ft) there was a significant increase in dispersion of blood flow (P less than 0.05) which implies an increase in intraregional inhomogeneity that more than counteracts the more uniform topographical distribution that occurs. Since breathing 100% O2 at 15,000 ft abolished the increased dispersion, the greater VA/Q mismatching seen during exercise at altitude may be related to pulmonary hypertension.

Nitric oxide and cardiopulmonary hemodynamics in Tibetan highlanders

2005 ◽  
Vol 99 (5) ◽  
pp. 1796-1801 ◽  
Author(s):  
Brian D. Hoit ◽  
Nancy D. Dalton ◽  
Serpil C. Erzurum ◽  
Daniel Laskowski ◽  
Kingman P. Strohl ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
High Altitude ◽  
Sea Level ◽  
Pulmonary Blood Flow ◽  
Geometric Mean ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Exhaled No

When O2 availability is reduced unavoidably, as it is at high altitude, a potential mechanism to improve O2 delivery to tissues is an increase in blood flow. Nitric oxide (NO) regulates blood vessel diameter and can influence blood flow. This field study of intrapopulation variation at high altitude tested the hypothesis that the level of exhaled NO (a summary measure of pulmonary synthesis, consumption, and transfer from cells in the airway) is directly proportional to pulmonary, and thus systemic, blood flow. Twenty Tibetan male and 37 female healthy, nonsmoking, native residents at 4,200 m (13,900 ft), with an average O2 saturation of hemoglobin of 85%, participated in the study. The geometric mean partial pressure of NO exhaled at a flow of 17 ml/s was 23.4 nmHg, significantly lower than that of a sea-level reference group. However, the rate of NO transfer out of the airway wall was seven times higher than at sea level, which implied the potential for vasodilation of the pulmonary blood vessels. Mean pulmonary blood flow (measured by cardiac index) was 2.7 ± 0.1 (SE) l/min, and mean pulmonary artery systolic pressure was 31.4 ± 0.9 (SE) mmHg. Higher exhaled NO was associated with higher pulmonary blood flow; yet there was no associated increase in pulmonary artery systolic pressure. The results suggest that NO in the lung may play a key beneficial role in allowing Tibetans at 4,200 m to compensate for ambient hypoxia with higher pulmonary blood flow and O2 delivery without the consequences of higher pulmonary arterial pressure.

Internal carotid and vertebral arterial flow velocity in men at high altitude

1987 ◽  
Vol 63 (1) ◽  
pp. 395-400 ◽  
Author(s):  
S. Y. Huang ◽  
L. G. Moore ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
A. J. Micco ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Flow Velocity ◽  
Sea Level ◽  
Internal Carotid ◽  
Hemoglobin Concentration ◽  
Subsequent Increase ◽  
O2 Transport ◽  
Flow Velocities

Cerebral blood flow increases at high altitude, but the mechanism of the increase and its role in adaptation to high altitude are unclear. We hypothesized that the hypoxemia at high altitude would increase cerebral blood flow, which would in turn defend O2 delivery to the brain. Noninvasive Doppler ultrasound was used to measure the flow velocities in the internal carotid and the vertebral arteries in six healthy male subjects. Within 2–4 h of arrival on Pikes Peak (4,300 m), velocities in both arteries were slightly and not significantly increased above sea-level values. By 18–44 h a peak increase of 20% was observed (combined P less than 0.025). Subsequently (days 4–12) velocities declined to values similar to those at sea level. At altitude the lowest arterial O2 saturation (SaO2) and the highest end-tidal PCO2 was observed on arrival. By day 4 and thereafter, when the flow velocities had returned toward sea-level values, hemoglobin concentration and SaO2 were increased over initial high-altitude values such that calculated O2 transport values were even higher than those at sea level. Although the cause of the failure for cerebral flow velocity to increase on arrival is not understood, the subsequent increase may act to defend brain O2 transport. With further increase in hemoglobin and SaO2 over time at high altitude, flow velocity returned to sea-level values.

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