METABOLIC ACIDOSIS OF THE CEREBROSPINAL FLUID ASSOCIATED WITH SUBARACHNOID HqMORRHAGE

The Lancet ◽  
1967 ◽  
Vol 289 (7497) ◽  
pp. 965-967 ◽  
Author(s):  
C FROMAN
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis

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.

Brain glutamate metabolism during metabolic alkalosis and acidosis

1992 ◽  
Vol 73 (6) ◽  
pp. 2552-2558 ◽  
Author(s):  
R. C. Ang ◽  
B. Hoop ◽  
H. Kazemi
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
De Novo ◽  
Respiratory Control ◽  
Gamma Aminobutyric Acid ◽  
Glutamate Metabolism ◽  
Acid Base ◽  
Transfer Rates ◽  
Normal Acid

Glutamate modifies ventilation by altering neural excitability centrally. Metabolic acid-base perturbations may also alter cerebral glutamate metabolism locally and thus affect ventilation. Therefore, the effect of metabolic acid-base perturbations on central nervous system glutamate metabolism was studied in pentobarbital-anesthetized dogs under normal acid-base conditions and during isocapnic metabolic alkalosis and acidosis. Cerebrospinal fluid transfer rates of radiotracer [13N]ammonia and of [13N]glutamine synthesized de novo via the reaction glutamate+NH3-->glutamine in brain glia were measured during normal acid-base conditions and after 90 min of acute isocapnic metabolic alkalosis and acidosis. Cerebrospinal fluid [13N]ammonia and [13N]glutamine transfer rates decreased in metabolic acidosis. Maximal glial glutamine efflux rate jm equals 85.6 +/- 9.5 (SE) mumol.l-1 x min-1 in all animals. No difference in jm was observed in metabolic alkalosis or acidosis. Mean cerebral cortical glutamate concentration was significantly lower in acidosis [7.01 +/- 0.45 (SE) mumol/g brain tissue] and tended to be larger in alkalosis, compared with 7.97 +/- 0.89 mumol/g in normal acid-base conditions. There was a similar change in cerebral cortical gamma-aminobutyric acid concentration. Within the limits of the present method and measurements, the results suggest that acute metabolic acidosis but not alkalosis reduces glial glutamine efflux, corresponding to changes in cerebral cortical glutamate metabolism. These results suggest that glutamatergic mechanisms may contribute to central respiratory control in metabolic acidosis.

Vasopressin in plasma and cerebrospinal fluid of dogs during hypoxia or acidosis

1984 ◽  
Vol 247 (4) ◽  
pp. E449-E455 ◽  
Author(s):  
B. C. Wang ◽  
W. D. Sundet ◽  
K. L. Goetz
Keyword(s):  
Mechanical Ventilation ◽  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Synergistic Effects ◽  
Muscle Paralysis ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Vasopressin Secretion ◽  
Slow Intravenous Infusion ◽  
Mild Hypoxia

Hypoxia and hypercapnia have been shown to cause an increase in the concentration of vasopressin in plasma, but their effects on vasopressin in cerebrospinal fluid (CSF) are not known. In addition, the effect of metabolic acidosis on plasma and CSF vasopressin has not been reported. In this study, plasma and CSF vasopressin levels were measured in anesthetized dogs subjected to either hypoxia, hypercapnia, or metabolic acidosis. Rate and depth of respiration were closely regulated with the aid of muscle paralysis and mechanical ventilation. Vasopressin increased markedly in both plasma and CSF during severe hypoxia (10% O2) and during hypercapnia (10% CO2) but did not change during either mild (15% O2) or moderate (12.5% O2) hypoxia. Although mild hypoxia by itself did not affect either plasma or CSF vasopressin, it did potentiate the increase in plasma and CSF vasopressin that was induced by severe hypercapnia, thus suggesting that hypoxia and hypercapnia may exert synergistic effects on vasopressin secretion. Metabolic acidosis produced by slow intravenous infusion of 1 N hydrochloric acid decreased arterial pH to values comparable to those induced by hypercapnia and increased vasopressin in plasma; CSF vasopressin was unchanged. These results are consistent with the concept that the source of vasopressin secreted into plasma may be different from that secreted into CSF.

Restoration of CSF [HCO3-] after its experimental lowering in normocapnic conditions

1979 ◽  
Vol 47 (2) ◽  
pp. 369-376 ◽  
Author(s):  
J. Weyne ◽  
H. Kazemi ◽  
I. Leusen
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Concentration Gradient ◽  
Intraventricular Injection ◽  
Bicarbonate Concentration ◽  
Brain Ventricles ◽  
Normal Plasma ◽  
Small Rise ◽  
The Brain

It is accepted that in hypercapnia the rise in cerebrospinal fluid bicarbonate concentration (CSF [HCO3-]) occurs because of local HCO3--generating mechanisms, dependent on carbonic anhydrase, as well as on diffusion of HCO3- from plasma. To investigate further the regulation of CSF [HCO3-], CSF HCO3- formation was studied under conditions of pure isocapnic CSF “metabolic” acidosis. In anesthetized normocapnic dogs CSF [HCO3-] was lowered to approximately 15 mmol/l by perfusing the brain ventricles with a low HCO3- solution for 45 min. In dogs with normal plasma [HCO3-], CSF [HCO3-] rose by approximately 7 mmol/l in 2 h after the end of the perfusion. Lowering plasma [HCO3-] to 10 mmol/l by infusing HCl, limited the CSF [HCO3-] rise to 2 mmol/l, indicating the importance of plasma HCO3- for the restoration of CSF [HCO3-]. The small and persistent rise of CSF [HCO3-] at low plasma [HCO3-] occurred against a concentration gradient with blood. Intraventricular injection of acetazolamide had no further effect on this small rise. It is concluded that under the conditions of our experiments the CSF [HCO3-] rise is significantly dependent on plasma [HCO3-] and the caronic anhydrase-dependent HCO3- generation in the CNS is less important.

Acid-Base Changes in Cerebrospinal Fluid of Infants with Metabolic Acidosis

1966 ◽  
Vol 274 (13) ◽  
pp. 719-721 ◽  
Author(s):  
Morris S. Albert ◽  
W.Joseph Rahill ◽  
Luis Vega ◽  
Robert W. Winters
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Acid Base

Cerebrospinal fluid ions in metabolic acidosis in dogs: effects of acetazolamide

1986 ◽  
Vol 61 (2) ◽  
pp. 633-639 ◽  
Author(s):  
S. Javaheri ◽  
J. Kennealy ◽  
C. D. Runck ◽  
R. G. Loudon ◽  
M. B. Pine ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Mechanical Ventilation ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Metabolic Acidosis ◽  
Control Group ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Group I ◽  
The Central Nervous System

We hypothesized that, during isosmotic isonatremic HCl acidosis with maintained isocapnia in cisternal cerebrospinal fluid (CSF), acetazolamide, by inhibiting carbonic anhydrase (CA) in the central nervous system (CNS), should produce an isonatric hyperchloric metabolic acidosis in CSF. Blood and CSF ions and acid-base variables were measured in two groups of anesthetized and paralyzed dogs with bilateral ligation of renal pedicles during 5 h of HCl acidosis (plasma [HCO3-] = 11 meq/l). Mechanical ventilation was regulated such that arterial PCO2 dropped and CSF Pco2 remained relatively constant. In group I (control group, n = 6), CSF [Na+] remained unchanged, [HCO3-] and strong ions difference (SID) fell, respectively, 6.1 and 5 meq/l, and [Cl-] rose 3.5 meq/l after 5 h of acidosis. In acetazolamide-treated animals, (group II, n = 7), CSF [Na+] remained unchanged, [HCO3-], and SID fell 11 and 7.1 meq/l, respectively, and [Cl-] rose 7.1 meq/l. We conclude that during HCl acidosis inhibition of CNS CA by acetazolamide induces an isonatric hyperchloric metabolic acidosis in CSF, which is more severe than that observed in controls.

Changes in brain ECF pH during metabolic acidosis and alkalosis: a microelectrode study

1983 ◽  
Vol 55 (6) ◽  
pp. 1849-1853 ◽  
Author(s):  
S. Javaheri ◽  
A. De Hemptinne ◽  
B. Vanheel ◽  
I. Leusen
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Extracellular Fluid ◽  
Acid Base ◽  
Brain Extracellular Fluid ◽  
Group I ◽  
Venous Pco2 ◽  
Anesthetized Dogs ◽  
Acute Metabolic Acidosis

We used pH-sensitive double-barreled microelectrodes to measure brain extracellular fluid (ECF) pH in anesthetized dogs during isocapnic infusion acidosis (HCl) and alkalosis (Na2CO3) of 45-60 min duration. The diameter of the tips of these electrodes varied from less than 1 to 27 micron and were placed 5 mm below the surface of the parietal cortex. In group I (metabolic acidosis, n = 5) mean plasma and brain ECF pH fell significantly by 0.221 and 0.025, respectively, with changes in brain ECF pH being 11.3% of those noted in plasma. In group II (metabolic alkalosis, n = 5) mean plasma and brain ECF pH rose significantly by 0.170 and 0.049, respectively, with changes in brain ECF pH being 28.8% of those noted in plasma. Mean arterial and sagittal venous PCO2 and cisternal cerebrospinal fluid (CSF) acid-base variables did not change significantly during acid or base infusion. We conclude that during transients of isocapnic metabolic acid-base perturbations ionic gradients exist between brain ECF and CSF and that changes in brain ECF pH measured by microelectrodes follow the changes in plasma pH. These pH changes may play an important role in respiratory adaptations of acute metabolic acidosis and alkalosis.

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