Chronic derangements of cerebrospinal fluid acid-base components in man

1962 ◽  
Vol 17 (6) ◽  
pp. 993-998 ◽  
Author(s):  
H. G. Pauli ◽  
C. Vorburger ◽  
F. Reubi
Keyword(s):  
Cerebrospinal Fluid ◽  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Fast Diffusion ◽  
Acid Base ◽  
Arterial Blood ◽  
Ion Gradient ◽  
Altitude Adaptation ◽  
Respiratory Centers ◽  
Stimulation Of

In a group of normal subjects a relative respiratory acidosis in the cerebrospinal fluid (CSF) as compared with arterial blood was found. There was no significant gradient for bicarbonate concentrations between the two compartments. In normal subjects under high-altitude adaptation, arterial and CSF respiratory alkalotic shifts were similar. A concomitant fall in bicarbonate levels was slightly less in CSF than in arterial blood. In a group of patients with uremic acidosis the arterial-cerebrospinal H ion gradient was reversed, as bicarbonate was significantly less reduced in CSF relative to arterial blood. Hemodialysis led to restitution of the relative respiratory acidosis in CSF. These findings seem to indicate fast diffusion of CO2 across the cerebrospinal-arterial barrier. In contrast, diffusion of bicarbonate and/or H ion appears to be delayed and incomplete. CSF acid-base components are not likely to correlate with stimulation of the respiratory centers under these conditions. Submitted on March 12, 1962

The relative roles of external and internal CO2versusH+ in eliciting the cardiorespiratory responses ofSalmo salarandSqualus acanthiasto hypercarbia

2001 ◽  
Vol 204 (22) ◽  
pp. 3963-3971 ◽  
Author(s):  
S. F. Perry ◽  
J. E. McKendry
Keyword(s):  
Cardiac Output ◽  
Sea Water ◽  
Buccal Cavity ◽  
Respiratory Acidosis ◽  
Systemic Resistance ◽  
Measured Variable ◽  
Cardiorespiratory Responses ◽  
Arterial Blood ◽  
Water Ph ◽  
Stimulation Of

SUMMARYFish breathing hypercarbic water encounter externally elevated PCO2 and proton levels ([H+]) and experience an associated internal respiratory acidosis, an elevation of blood PCO2 and [H+]. The objective of the present study was to assess the potential relative contributions of CO2versus H+ in promoting the cardiorespiratory responses of dogfish (Squalus acanthias) and Atlantic salmon (Salmo salar) to hypercarbia and to evaluate the relative contributions of externally versus internally oriented receptors in dogfish.In dogfish, the preferential stimulation of externally oriented branchial chemoreceptors using bolus injections (50 ml kg–1) of CO2-enriched (4 % CO2) sea water into the buccal cavity caused marked cardiorespiratory responses including bradycardia (–4.1±0.9 min–1), a reduction in cardiac output (–3.2±0.6 ml min–1 kg–1), an increase in systemic vascular resistance (+0.3±0.2 mmHg ml min–1 kg–1), arterial hypotension (–1.6±0.2 mmHg) and an increase in breathing amplitude (+0.3±0.09 mmHg) (means ± s.e.m., N=9–11). Similar injections of CO2-free sea water acidified to the corresponding pH of the hypercarbic water (pH 6.3) did not significantly affect any of the measured cardiorespiratory variables (when compared with control injections). To preferentially stimulate putative internal CO2/H+ chemoreceptors, hypercarbic saline (4 % CO2) was injected (2 ml kg–1) into the caudal vein. Apart from an increase in arterial blood pressure caused by volume loading, internally injected CO2 was without effect on any measured variable.In salmon, injection of hypercarbic water into the buccal cavity caused a bradycardia (–13.9±3.8 min–1), a decrease in cardiac output (–5.3±1.2 ml min–1 kg–1), an increase in systemic resistance (0.33±0.08 mmHg ml min–1 kg–1) and increases in breathing frequency (9.7±2.2 min–1) and amplitude (1.2±0.2 mmHg) (means ± s.e.m., N=8–12). Apart from a small increase in breathing amplitude (0.4±0.1 mmHg), these cardiorespiratory responses were not observed after injection of acidified water.These results demonstrate that, in dogfish and salmon, the external chemoreceptors linked to the initiation of cardiorespiratory responses during hypercarbia are predominantly stimulated by the increase in water PCO2 rather than by the accompanying decrease in water pH. Furthermore, in dogfish, the cardiorespiratory responses to hypercarbia are probably exclusively derived from the stimulation of external CO2 chemoreceptors, with no apparent contribution from internally oriented receptors.

The effects of enforced activity on ventilation, circulation and blood acid-base balance in the aquatic gill-less urodele, Cryptobranchus alleganiensis; a comparison with the semi-terrestrial anuran, Bufo marinus

1980 ◽  
Vol 84 (1) ◽  
pp. 289-302
Author(s):  
R. G. Boutilier ◽  
D. G. McDonald ◽  
D. P. Toews
Keyword(s):  
Recovery Period ◽  
Respiratory Acidosis ◽  
Bufo Marinus ◽  
Acid Base Balance ◽  
Acid Base ◽  
Post Exercise ◽  
Arterial Blood ◽  
Cryptobranchus Alleganiensis ◽  
Base Balance ◽  
Lower Magnitude

A combined respiratory and metabolic acidosis occurs in the arterial blood immediately following 30 min of strenuous activity in the predominantly skin-breathing urodele, Cryptobranchus alleganiensis, and in the bimodal-breathing anuran, Bufo marinus, at 25 degrees C. In Bufo, the bulk of the post-exercise acidosis is metabolic in origin (principally lactic acid) and recovery is complete within 4-8 h. In the salamander, a lower magnitude, longer duration, metabolic acid component and a more pronounced respiratory acidosis prolong the recovery period for up to 22 h post-exercise. It is suggested that fundamental differences between the dominant sites for gas exchange (pulmonary versus cutaneous), and thus in the control of respiratory acid-base balance, may underline the dissimilar patterns of recovery from exercise in these two species.

Acid-Base Relationships in the Blood of the Toad, Bufo Marinus: I. The Effects of Environmental CO2

1979 ◽  
Vol 82 (1) ◽  
pp. 331-344 ◽  
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS
Keyword(s):  
Respiratory Acidosis ◽  
Initial Response ◽  
Untreated Animal ◽  
Abrupt Increase ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Ph Values ◽  
Arterial Blood ◽  
Toad Bufo ◽  
Ambient Co2

An abrupt increase in ambient CO2, resulted in a marked respiratory acidosis which took place within 30 min. During this time there was a considerable reduction in the PCO2. difference between arterial blood and inspired gas caused by an increase in ventilations. Prolonged CO2 exposure (24 h) showed that there was some compensation for the acidosis in that plasma bicarbonate concentrations increased substantially. At the same time, however, the PCO2 of arterial blood always rose so that the net result was usually only a small increase in pH. Upon return to air, the blood was backtitrated along a buffer line elevated above and parallel to that seen during the initial response to hypercapnia. The fall in arterial blood PCO2, during the early stages of recovery often led to pH values higher than those seen in the untreated animal. After 48 h in air, recovery had gone further with PCO2 pH and [HCO3-] levels approaching but rarely reaching the pre-exposure values.

Stability of cerebrospinal fluid pH in chronic acid-base disturbances in blood

1965 ◽  
Vol 20 (3) ◽  
pp. 443-452 ◽  
Author(s):  
R. A. Mitchell ◽  
C. T. Carman ◽  
J. W. Severinghaus ◽  
B. W. Richardson ◽  
M. M. Singer ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Active Transport ◽  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Respiratory Alkalosis ◽  
Regulation Of Respiration ◽  
Respiratory Drive ◽  
Acid Base ◽  
Peripheral Chemoreceptors ◽  
Mean Values

In chronic acid-base disturbances, CSF pH was generally within the normal limits (7.30–7.36 units, being the range including two standard deviations of 12 normal subjects). The mean values of CSF and arterial pHH, respectively, were: 1) metabolic alkalosis, 7.337 and 7.523; 2) metabolic acidosis, 7.315 and 7.350; 3) respiratory alkalosis, 7.336 and 7.485; and 4) respiratory acidosis (untreated), 7.314 and 7.382. Other investigators report similar values. The constancy of CSF pH cannot be explained by a poorly permeable blood-CSF barrier in chronic metabolic acidosis and alkalosis, nor can it be explained by respiratory compensation. It cannot be explained by renal compensation in respiratory alkalosis (high altitude for 8 days), although it may be explained by renal compensation in respiratory acidosis. The former three states suggest that active transport regulation of CSF pH is a function of the blood-CSF barrier. Since CSF pH is constant, so also must that portion of the respiratory drive originating in the superficial medullary respiratory chemoreceptors be constant. Ventilation changes in chronic acid-base disturbances thus may result from changes in the activity of peripheral chemoreceptors, in response to changes in arterial pH, arterial PO2, and possibly in neuromuscular receptors. regulation of respiration; medullary respiratory; chemoreceptors; peripheral chemoreceptors; metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; active transport; blood-brain barrier; pregnancy Submitted on July 27, 1964

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.

scholarly journals ACID-BASE CHANGES IN ARTERIAL BLOOD AND CEREBROSPINAL FLUID DURING CRANIOTOMY AND HYPERVENTILATION

1974 ◽  
Vol 46 (4) ◽  
pp. 263-267 ◽  
Author(s):  
T.V. CAMPKIN ◽  
R.G. BARKER ◽  
M PABARI ◽  
L.H. GROVE
Keyword(s):  
Cerebrospinal Fluid ◽  
Acid Base ◽  
Arterial Blood

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

Anesthetic effects on liver and muscle glycogen concentrations: rest and postexercise

1989 ◽  
Vol 66 (6) ◽  
pp. 2895-2900 ◽  
Author(s):  
T. I. Musch ◽  
B. S. Warfel ◽  
R. L. Moore ◽  
D. R. Larach
Keyword(s):  
Skeletal Muscles ◽  
Respiratory Acidosis ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Acid Base ◽  
Arterial Lactate ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Gastrocnemius Muscles

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.

Hyperoxia of cerebral venous blood and cisternal cerebrospinal fluid following arterial air embolism

1972 ◽  
Vol 37 (1) ◽  
pp. 30-35 ◽  
Author(s):  
Norval M. Simms ◽  
Don M. Long ◽  
James H. Matthews ◽  
Shelley N. Chou
Keyword(s):  
Cerebrospinal Fluid ◽  
Oxygen Tension ◽  
Venous Blood ◽  
Air Embolism ◽  
Carbon Dioxide Tension ◽  
Acid Base ◽  
Content Type ◽  
Arterial Blood ◽  
Base Parameters ◽  
The Right

✓ Oxygen tension and acid-base parameters of cerebral venous blood and cisternal cerebrospinal fluid, as well of femoral arterial blood, were studied in 14 dogs following injection of varying amounts of room air into the right vertebral artery. Acute elevations in oxygen tension were demonstrated in both cerebral venous blood and CSF, whereas hypoxemia occurred concomitantly in systemic arterial blood. Post-embolic increases in carbon dioxide tension with reciprocal diminutions in pH were evident in all sampling sites. The pathophysiological bases for these air-induced alterations are discussed.

scholarly journals The effects of post-operative oxygen supply on blood oxygenation and acid-base status in rats anaesthetized with fentanyl/fluanisone and midazolam

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255829
Author(s):  
Leander Gaarde ◽  
Stefanie Kolstrup ◽  
Peter Bollen
Keyword(s):  
Oxygen Saturation ◽  
Oxygen Supply ◽  
Respiratory Acidosis ◽  
Blood Oxygenation ◽  
Acid Base ◽  
Blood Oxygen Saturation ◽  
Arterial Blood ◽  
Post Operative Period ◽  
Significant Difference ◽  
Acid Base Status

In anaesthetic practice the risk of hypoxia and arterial blood gas disturbances is evident, as most anaesthetic regimens depress the respiratory function. Hypoxia may be extended during recovery, and for this reason we wished to investigate if oxygen supply during a one hour post-operative period reduced the development of hypoxia and respiratory acidosis in rats anaesthetized with fentanyl/fluanisone and midazolam. Twelve Sprague Dawley rats underwent surgery and were divided in two groups, breathing either 100% oxygen or atmospheric air during a post-operative period. The peripheral blood oxygen saturation and arterial acid-base status were analyzed for differences between the two groups. We found that oxygen supply after surgery prevented hypoxia but did not result in a significant difference in the blood acid-base status. All rats developed respiratory acidosis, which could not be reversed by supplemental oxygen supply. We concluded that oxygen supply improved oxygen saturation and avoided hypoxia but did not have an influence on the acid-base status.

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