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.

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-].

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.

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.

The Impact of Peritonitis on Peritoneal and Systemic Acid-Base Status of Patients on Continuous Ambulatory Peritoneal Dialysis

1994 ◽  
Vol 14 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Jacques J. Sennesael ◽  
Godelieve C. De Smedt ◽  
Patricia Van der Niepen ◽  
Dierik L. Verbeelen
Keyword(s):  
Staphylococcus Aureus ◽  
Peritoneal Dialysis ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Acid Base ◽  
Gram Positive ◽  
Gram Negative ◽  
Arterial Blood ◽  
Blood Ph ◽  
Acid Base Status ◽  
And Staphylococcus Aureus

Objective To assess the possible effects of peritonitis on peritoneal and systemic acid-base status. Design pH, pCO2, lactate, and total leukocyte and differential count were simultaneously determined in the overnight dwell peritoneal dialysis effluent (PDE) and arterial blood in noninfected patients (controls) and on days 1, 3, and 5 from the onset of peritonitis. Setting University multidisciplinary dialysis program. Patients Prospective analysis of 63 peritonitis episodes occurring in 30 adult CAPD patients in a single center. Results In controls, mean (±SD) acid-base parameters were pH 7.41 ±0.05, pCO2 43.5±2.6 mm Hg, lactate 2.5±1.5 mmol/L in the PDE, and pH 7.43±0.04, PaCO2 36.8±3.8 mm Hg, lactate 1.4±0.7 mmol/L in the blood. In sterile (n=6), gram-positive (n=34), and Staphylococcus aureus (n=9) peritonitis PDE pH's on day 1 were, respectively, 7. 29±0.07, 7. 32±0.07, and 7.30±0.08 (p<0.05 vs control). In gram -negative peritonitis (n=14) PDE pH was 7.21 ±0.08 (p<0.05 vs all other groups). A two-to-threefold increase in PDE lactate was observed in all peritonitis groups, but a rise in pCO2 was only seen in gram -negative peritonitis. Acid-base profile of PDE had returned to control values by day 3 in sterile, gram -positive and Staphylococcus aureus peritonitis and by day 5 in gramnegative peritonitis. Despite a slight increase in plasma lactate on the first day of peritonitis, arterial blood pH was not affected by peritonitis. Conclusion PDE pH is decreased in continuous ambulatory peritoneal dialysis (CAPD) peritonitis, even in the absence of bacterial growth. In gram-negative peritonitis, PDE acidosis is more pronounced and prolonged, and pCO2 is markedly increased. Arterial blood pH is not affected by peritonitis.

Acid-Base Relationships in the Blood of the Toad, Bufo Marinus: II. The Effects of Dehydration

1979 ◽  
Vol 82 (1) ◽  
pp. 345-355
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS
Keyword(s):  
Water Loss ◽  
Respiratory Acidosis ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
Acid Base Status ◽  
Toad Bufo ◽  
Circulating Levels ◽  
Bladder Urine ◽  
Co2 Excretion

Cutaneous CO2 excretion is reduced as the skin dries during dehydration but an increase in breath frequency acts to regulate the arterial blood Pcoco2 and thus pHα. Moreover, the toad does not urinate and water is reabsorbed from the bladder to replace that lost by evaporation at the skin and lung surfaces. The animal does, however, produce a very acid bladder urine to conserve circulating levels of plasma [HCO3-] and this together with an increased ventilation effectively maintains the blood acid-base status for up to 48 h of dehydration in air. Water loss and acid production are presumably also reduced by the animal's behaviour; animals remain still, in a crouched position or in a pile if left in groups. Dehydrated toads are less able than hydrated toads to regulate blood pH during hypercapnia: they hyperventilate and mobilize body bicarbonate stores in much the same fashion as hydrated animals but due to the restrictions on cutaneous CO2 excretion and renal output, there is comparatively little reduction in the PCOCO2 difference between arterial blood and inspired gas thereby resulting in a more severe respiratory acidosis. These factors further contribute to the persistent acidosis which continues even when the animals are returned to air.

A mathematical model of blood-interstitial acid-base balance: application to dilution acidosis and acid-base status

2011 ◽  
Vol 110 (4) ◽  
pp. 988-1002 ◽  
Author(s):  
Matthew B. Wolf ◽  
Edward C. DeLand
Keyword(s):  
Erythrocyte Membrane ◽  
Interstitial Fluid ◽  
Equilibrium Distribution ◽  
Base Excess ◽  
Acid Base ◽  
Mobile Species ◽  
Blood Ph ◽  
Base Disorder ◽  
Model Predictions ◽  
Acid Base Status

We developed mathematical models that predict equilibrium distribution of water and electrolytes (proteins and simple ions), metabolites, and other species between plasma and erythrocyte fluids (blood) and interstitial fluid. The models use physicochemical principles of electroneutrality in a fluid compartment and osmotic equilibrium between compartments and transmembrane Donnan relationships for mobile species. Across the erythrocyte membrane, the significant mobile species Cl−is assumed to reach electrochemical equilibrium, whereas Na+and K+distributions are away from equilibrium because of the Na+/K+pump, but movement from this steady state is restricted because of their effective short-term impermeability. Across the capillary membrane separating plasma and interstitial fluid, Na+, K+, Ca2+, Mg2+, Cl−, and H+are mobile and establish Donnan equilibrium distribution ratios. In each compartment, attainment of equilibrium by carbonates, phosphates, proteins, and metabolites is determined by their reactions with H+. These relationships produce the recognized exchange of Cl−and bicarbonate across the erythrocyte membrane. The blood submodel was validated by its close predictions of in vitro experimental data, blood pH, pH-dependent ratio of H+, Cl−, and HCO3−concentrations in erythrocytes to that in plasma, and blood hematocrit. The blood-interstitial model was validated against available in vivo laboratory data from humans with respiratory acid-base disorders. Model predictions were used to gain understanding of the important acid-base disorder caused by addition of saline solutions. Blood model results were used as a basis for estimating errors in base excess predictions in blood by the traditional approach of Siggaard-Andersen (acid-base status) and more recent approaches by others using measured blood pH and Pco2values. Blood-interstitial model predictions were also used as a basis for assessing prediction errors of extracellular acid-base status values, such as by the standard base excess approach. Hence, these new models can give considerable insight into the physicochemical mechanisms producing acid-base disorders and aid in their diagnoses.

scholarly journals Damage to the gastric epithelium activates cellular bicarbonate secretion via SLC26A9 Cl−/HCO3−exchange

2010 ◽  
Vol 299 (1) ◽  
pp. G255-G264 ◽  
Author(s):  
Elise S. Demitrack ◽  
Manoocher Soleimani ◽  
Marshall H. Montrose
Keyword(s):  
Interstitial Fluid ◽  
Gastric Epithelium ◽  
Acid Base ◽  
Surface Ph ◽  
Two Photon ◽  
Acid Base Status ◽  
Genetic Deletion ◽  
Knockout Animals ◽  
Tissue Compartments

Gastric surface pH (pHo) transiently increases in response to focal epithelial damage. The sources of that increase, either from paracellular leakage of interstitial fluid or transcellular acid/base fluxes, have not been determined. Using in vivo microscopy approaches we measured pHowith Cl-NERF, tissue permeability with intravenous fluorescent-dextrans to label interstitial fluid (paracellular leakage), and gastric epithelial intracellular pH (pHi) with SNARF-5F (cellular acid/base fluxes). In response to two-photon photodamage, we found that cell-impermeant dyes entered damaged cells from luminal or tissue compartments, suggesting a possible slow transcellular, but not paracellular, route for increased permeability after damage. Regarding cytosolic acid/base status, we found that damaged cells acidified (6.63 ± 0.03) after photodamage, compared with healthy surface cells both near (7.12 ± 0.06) and far (7.07 ± 0.04) from damage ( P < 0.05). This damaged cell acidification was further attenuated with 20 μM intravenous EIPA (6.34 ± 0.05, P < 0.05) but unchanged by addition of 0.5 mM luminal H2DIDS (6.64 ± 0.08, P > 0.05). Raising luminal pH did not realkalinize damaged cells, suggesting that the mechanism of acidification is not attributable to leakiness to luminal protons. Inhibition of apical HCO3−secretion with 0.5 mM luminal H2DIDS or genetic deletion of the solute-like carrier 26A9 (SLC26A9) Cl−/HCO3−exchanger blocked the pHoincrease normally observed in control animals but did not compromise repair of damaged tissue. Addition of exogenous PGE2significantly increased pHoin wild-type, but not SLC26A9 knockout, animals, suggesting that prostaglandin-stimulated HCO3−secretion is fully mediated by SLC26A9. We conclude that cellular HCO3−secretion, likely through SLC26A9, is the dominant mechanism whereby surface pH transiently increases in response to photodamage.

scholarly journals Slowly Changing Bioelectric Potentials Associated With the Blood-Brain Barrier

1958 ◽  
Vol 195 (1) ◽  
pp. 7-22 ◽  
Author(s):  
Robert D. Tschirgi ◽  
J. Langdon Taylor
Keyword(s):  
Cerebral Cortex ◽  
Blood Brain Barrier ◽  
Interstitial Fluid ◽  
Brain Barrier ◽  
Membrane Diffusion ◽  
Arterial Blood ◽  
Blood Ph ◽  
Blood Brain ◽  
The Central Nervous System ◽  
Bioelectric Potentials

A slowly changing bioelectric potential difference (P.D.) is measured in rats, rabbits, cats and dogs between various regions of the central nervous system (CNS) and the blood within the jugular vein. It is shown that the CNS-blood P.D. is very sensitive to alterations in alveolar CO2 tension, but this relationship is dependent upon the H+ concentration rather than CO2 per se. Whereas increasing intravenous H+ concentration increases CNS positivity, topical application of acid solutions directly to the cerebral cortex decreases CNS positivity. The same relationship is found for intravenous and topical K+. Anoxia and circulatory failure produce CNS negative deflections, often exceeding 15 mv, which do not return to zero for over 24 hours after death. Simultaneous measurements of arterial blood pH, cerebral cortex pH and CNS-blood P.D. reveal the following relationship among these variables: ΔP.D. = κ Δ log10 [H+]a/[H+]i where [H+]a is the H+ concentration of the arterial blood and [H+]i is the H+ concentration of the CNS interstitial fluid. For the CNS-blood P.D. between cerebral cortex and jugular blood of rabbits and rats, κ is found to be 29 ± 5. These results are interpreted as indicating a source of emf across the pan-vascular blood-brain barrier which resembles a membrane diffusion potential. The blood-brain barrier is postulated to be more permeable to H+ and K+ than to anions and other cations.

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