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

Acid-base balance at high altitude in lowlanders and indigenous highlanders

2022 ◽  
Author(s):  
Michael M. Tymko ◽  
Christopher K. Willie ◽  
Connor A. Howe ◽  
Ryan L. Hoiland ◽  
Rachel Stone ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Respiratory Alkalosis ◽  
Indigenous Populations ◽  
Acid Base Balance ◽  
Acid Base ◽  
Altitude Exposure ◽  
Arterial Blood ◽  
Blood Ph ◽  
Base Balance

High-altitude exposure results in a hyperventilatory-induced respiratory alkalosis followed by renal compensation (bicarbonaturia) to return arterial blood pH(a) toward sea-level values. However, acid-base balance has not been comprehensively examined in both lowlanders and indigenous populations - where the latter are thought to be fully adapted to high-altitude. The purpose of this investigation was to compare acid-base balance between acclimatizing lowlanders, and Andean and Sherpa highlanders at various altitudes (~3,800, ~4,300, and ~5,000 m). We compiled data collected across five independent high-altitude expeditions and report the following novel findings: 1) at 3,800 m, Andeans (n=7) had elevated pHa compared to Sherpas (n=12; P<0.01), but not to lowlanders (n=16; nine days acclimatized; P=0.09); 2) at 4,300 m, lowlanders (n=16; 21 days acclimatized) had elevated pHa compared to Andeans (n=32) and Sherpas (n=11; both P<0.01), and Andeans had elevated pHa compared to Sherpas (P=0.01); and 3) at 5,000 m, lowlanders (n=16; 14 days acclimatized) had higher pHa compared to both Andeans (n=66) and Sherpas (n=18; P<0.01, and P=0.03, respectively), and Andean and Sherpa highlanders had similar blood pHa (P=0.65). These novel data characterize acid-base balance acclimatization and adaptation to various altitudes in lowlanders and indigenous highlanders.

Respiratory control at high altitude suggesting active transport regulation of CSF pH

1963 ◽  
Vol 18 (6) ◽  
pp. 1155-1166 ◽  
Author(s):  
J. W. Severinghaus ◽  
R. A. Mitchell ◽  
B. W. Richardson ◽  
M. M. Singer
Keyword(s):  
Sea Level ◽  
Active Transport ◽  
Regulation Of Respiration ◽  
Level Control ◽  
Response Curves ◽  
Peripheral Chemoreceptor ◽  
Mean Values ◽  
Arterial Blood ◽  
Ventilatory Drive ◽  
Four Levels

The role of CSF pH and HCO–3 ion in stimulating respiration was studied in four men during acclimatization from sea level to 3,800 m for 8 days. Mean values for sea level control, 2nd day and 8th day at altitude were, for CSF 7.328, 7.338, and 7.336, and for arterial blood 7.424, 7.485, and 7.484. Ventilatory response to four levels of alveolar CO2 was determined while subjects breathed high oxygen to eliminate peripheral chemoreceptor drive, and for each value of PaCOCO2, arterial and CSF pH were computed. The displacement of the ventilation response curves at altitude from the sea level curves was: -10 mm Hg PaCOCO2, + 0.06 pH unit for arterial blood, but -0.01 for CSF pH. CSF HCO3 was 4–5 mEq/liter lower than control within 1–2 days at altitude, whereas renal buffer base excretion only reduced blood standard bicarbonate 1 mEq/liter after a week. CSF chloride and lactate rose about 6 and 1 mEq/liter. Thus, medullary respiratory chemoreceptor drive, initially reduced at altitude by hyperventilation alkalosis, is restored to normal during acclimatization by reduction in CSF HCO3, the incremental ventilatory drive being supplied by peripheral chemoreceptors. The blood-CSF barrier appears to respond to the initial hyperventilation alkalosis by actively reducing CSF HCO3; the data suggest that CSF pH is thus regulated by active transport by the blood-CSF barrier. altitude acclimatization; blood brain barrier; regulation of respiration Submitted on December 17, 1962

Incomplete compensation of CSF [H+] in man during acclimatization to high altitude (48300 M)

1975 ◽  
Vol 38 (6) ◽  
pp. 1067-1072 ◽  
Author(s):  
H. V. Forster ◽  
J. A. Dempsey ◽  
L. W. Chosy
Keyword(s):  
Cerebrospinal Fluid ◽  
Time Course ◽  
Chronic Hypoxia ◽  
Acid Base ◽  
Healthy Men ◽  
Arterial Blood ◽  
Blood Ph ◽  
Acid Base Status ◽  
Normoxic Control ◽  
Lumbar Spinal

This study has assessed the regulation of arterial blood and cerebrospinal fluid acid-base status in seven healthy men, at 250 m altitude and after 5 and 10–11 days sojourn at 4,300 m altitude (PaO2 = 39 mmHg day 1 to 48 mmHg day 11). We assumed that observed changes in lumbar spinal fluid acid-base status paralleled those in cisternal CSF, under these relatively steady-state conditions. Ventilatory acclimatization during the sojourn (-14 mmHg PaCO2 at day 11) was accompanied by: 1) reductions in [HCO3-] (-5 to -7 meq/1) which were similar in arterial blood and CSF; 2) substantial, yet incomplete, compensation (70–75%) of both CSF and blood pH; and 3) a level of CSF pH which was maintained significantly alkaline (+0.05 +/- 0.01) to normoxic control values. These data at 4,300 m confirmed and extended our previous findings for more moderate conditions of chronic hypoxia. It was postulated that the magnitude and time course of pH compensation in the CSF during chronic hypoxia and/or hypocapnia are determined by corresponding changes in plasma [HCO2-].

Cerebral interstitial fluid acid-base status follows arterial acid-base perturbations

1982 ◽  
Vol 53 (6) ◽  
pp. 1551-1555 ◽  
Author(s):  
D. G. Davies ◽  
W. F. Nolan
Keyword(s):  
Cerebrospinal Fluid ◽  
New Zealand ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Ph Probe ◽  
Arterial Blood ◽  
Blood Ph ◽  
New Zealand White Rabbits ◽  
Acid Base Status

Cerebral interstitial fluid (ISF) pH of ventral medulla or thalamus, cisternal cerebrospinal fluid (CSF) pH, and arterial blood pH, PCO2, and [HCO-3] were measured in chloralose-urethan-anesthetized, gallamine-paralyzed New Zealand White rabbits during 30-min episodes of either HCl or NaHCO3 intravenous infusions. ISF pH was measured continuously with glass microelectrodes (1- to 2-microns tip diameter). Cisternal CSF pH was measured continuously with an indwelling pH probe (1-mm tip diameter). Both ventral medullary and thalamic ISF [H+] changed significantly, whereas arterial PCO2 remained constant. CSF [H+] did not change. We conclude from these data that 1) changes in blood acid-base conditions are rapidly reflected in cerebral ISF and 2) transient differences in [H+] and [HCO-3] can exist between cerebral ISF and CSF.

scholarly journals Effects of External Acidification on the Blood Acid-Base Status and Ion Concentrations of Lamprey

1988 ◽  
Vol 136 (1) ◽  
pp. 351-361
Author(s):  
LEONA MATTSOFF ◽  
MIKKO NIKINMAA
Keyword(s):  
High Sensitivity ◽  
Co2 Concentration ◽  
Acid Base ◽  
Ion Concentrations ◽  
Ph Response ◽  
Ph Values ◽  
Blood Ph ◽  
Acid Base Status ◽  
The Difference ◽  
K Concentration

We studied the effects of acute external acidification on the acid-base status and plasma and red cell ion concentrations of lampreys. Mortality was observed within 24 h at pH5 and especially at pH4. The main reason for the high sensitivity of lampreys to acid water appears to be the large drop in blood pH: 0.6 and 0.8 units after 24 h at pH5 and pH4, respectively. The drop of plasma pH is much larger than in teleost fishes exposed to similar pH values. The difference in the plasma pH response between lampreys and teleosts probably results from the low buffering capacity of lamprey blood, since red cells cannot participate in buffering extracellular acid loads. Acidification also caused a decrease in both Na+ and C− concentrations and an elevation in K+ concentration of plasma. The drop in plasma Na+ concentration occurred faster than the drop in plasma Cl− concentration which, in turn, coincided with the decrease in total CO2 concentration of the blood.

Role of peripheral chemoreceptors and central chemosensitivity in the regulation of respiration and circulation.

1982 ◽  
Vol 100 (1) ◽  
pp. 23-40 ◽  
Author(s):  
R G O'Regan ◽  
S Majcherczyk
Keyword(s):  
The Body ◽  
Ion Concentration ◽  
Regulation Of Respiration ◽  
Acid Base Balance ◽  
Acid Base ◽  
Vascular Effects ◽  
Peripheral Chemoreceptor ◽  
Hydrogen Ion Concentration ◽  
Central Chemosensitivity ◽  
Base Balance

Adjustments of respiration and circulation in response to alterations in the levels of oxygen, carbon dioxide and hydrogen ions in the body fluids are mediated by two distinct chemoreceptive elements, situated peripherally and centrally. The peripheral arterial chemoreceptors, located in the carotid and aortic bodies, are supplied with sensory fibres coursing in the sinus and aortic nerves, and also receive sympathetic and parasympathetic motor innervations. The carotid receptors, and some aortic receptors, are essential for the immediate ventilatory and arterial pressure increases during acute hypoxic hypoxaemia, and also make an important contribution to respiratory compensation for acute disturbances of acid-base balance. The vascular effects of peripheral chemoreceptor stimulation include coronary vasodilation and vasoconstriction in skeletal muscle and the splanchnic area. The bradycardia and peripheral vasoconstriction during carotid chemoreceptor stimulation can be lessened or reversed by effects arising from a concurrent hyperpnoea. Central chemoreceptive elements respond to changes in the hydrogen ion concentration in the interstitial fluid in the brain, and are chiefly responsible for ventilatory and circulatory adjustments during hypercapnia and chronic disturbances of acid-base balance. The proposal that the neurones responsible for central chemoreception are located superficially in the ventrolateral portion of the medulla oblongata is not universally accepted, mainly because of a lack of convincing morphological and electrophysiological evidence. Central chemosensitive structures can modify peripheral chemoreceptor responses by altering discharges in parasympathetic and sympathetic nerves supplying these receptors, and such modifications could be a factor contributing to ventilatory unresponsiveness in mild hypoxia. Conversely, peripheral chemoreceptor drive can modulate central chemosensitivity during hypercapnia.

ERRATA

PEDIATRICS ◽  
1980 ◽  
Vol 65 (5) ◽  
pp. 1006-1006
Keyword(s):  
Metabolic Acidosis ◽  
Diagnostic Approach ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
P 351 ◽  
Normal Acid

In the article "A Diagnostic Approach to Metabolic Acidosis in Children" by Kappy and Morrow (Pediatrics 65:351-356, 1980) on p 351 under "Normal Acid-Base Physiology" the normal arterial blood pH is maintained at 7.40 (H+ = 39.8 nEq/liter not mEq/liter.

Acid-Base Regulation Following Exhaustive Exercise: A Comparison Between Freshwaterand Sea Water-Adapted Rainbow Trout (Salmo Gairdneri)

1989 ◽  
Vol 141 (1) ◽  
pp. 407-418 ◽  
Author(s):  
Y. TANG ◽  
D. G. McDONALD ◽  
R. G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
Sea Water ◽  
Environmental Water ◽  
Exhaustive Exercise ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Genetic Stock ◽  
Arterial Blood ◽  
Blood Ph ◽  
Counter Ions

Blood acid-base regulation following exhaustive exercise was investigated in freshwater- (FW) and seawater- (SW) adapted rainbow trout (Salmo gairdneri) of the same genetic stock. Following exhaustive exercise at 10°C, both FW and SW trout displayed a mixed respiratory and metabolic blood acidosis. However, in FW trout the acidosis was about double that of SW trout and arterial blood pH took twice as long to correct. These SW/FW differences were related to the relative amounts of net H+ equivalent excretion to the environmental water, SW trout excreting five times as much as FW trout. The greater H+ equivalent excretion in SW trout may be secondary to changes in the gills that accompany the adaptation from FW to SW. It may also be related to the higher concentrations of HCO3− as well as other exchangeable counter-ions (Na+ and Cl−) in the external medium in SW compared to FW.

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis

1981 ◽  
Vol 51 (2) ◽  
pp. 276-281 ◽  
Author(s):  
S. Javaheri ◽  
A. Clendening ◽  
N. Papadakis ◽  
J. S. Brody
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Surface Ph ◽  
Brain Surface ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean ◽  
The Brain

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

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