Distribution of H+ and HCO3 minus between CSF and blood during metabolic alkalosis in dogs

1975 ◽  
Vol 228 (4) ◽  
pp. 1141-1144 ◽  
Author(s):  
EG Pavlin ◽  
ttf Hornbein
Keyword(s):  
Cerebrospinal Fluid ◽  
Steady State ◽  
Metabolic Alkalosis ◽  
Extracellular Fluid ◽  
Ion Distribution ◽  
Brain Extracellular Fluid ◽  
Dc Potential ◽  
Arterial Plasma ◽  
Lumbar Cerebrospinal Fluid

In anesthetized, paralyzed dogs ventilated to maintain a normal PaCO2, metabolic alkalosis was induced and held constant over 6 h by infusion of sodium bicarbonate. Determination of pH, PCO2, (HCO3 minus), and (lactate) in cisternal and lumbar cerebrospinal fluid (CSF) and in arterial plasma together with measurement of the CSF/plasma DC potential differences permitted calculation of the electrochemical potential difference (mu) for H+ and HCO3 minus; measurements were made prior to induction of metabolic alkalosis at pHa equal to 7.40, as soon after induction as stable arterial values were achieved and 3, 4.5, and 6 h thereafter. A steady state for ion distribution was reached by 4.5 h. Values of mu for H+ and HCO3 minus returned to +0.1 and +0.9 mV of control at 6 h for cisternal CSF and +0.6 and minus 0.4 mV for lumbar CSF. This return of muH+ and muHCO3 minus close to control in the steady state is compatible with passive distribution of these ions between brain extracellular fluid and blood.

Distribution of H+ and HCO3 minus between CSF and blood during respiratory acidosis in dogs

1975 ◽  
Vol 228 (4) ◽  
pp. 1145-1148 ◽  
Author(s):  
EG Pavlin ◽  
TF Hornbein
Keyword(s):  
Steady State ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Potential Difference ◽  
Ion Distribution ◽  
Acid Base ◽  
Mechanically Ventilated ◽  
Brain Extracellular Fluid ◽  
Dc Potential ◽  
Arterial Plasma

To evaluate the regulation of (H+) and (HCO3 minus) in brain extracellular fluid during respiratory acidosis, the changes in cisternal and lumbar CSF acid-base state were assessed in six anteshetized, paralyzed, mechanically ventilated dogs rendered hypercapnic by increase in FIco2. Arterial (HCO3 minus) was held constant. The electrochemical potential difference (mu) between CSF and blood for H+ and HCO3 minus was calculated from values for (H+) and (HCO3 minus) in CSF and arterial plasma and the simultaneously measured CSF/plasma DC potential difference. Measurements were made at pHa equal to 7.40, after stable arterial values of pHa of about 7.2 were attained and 3, 4.5, and 6 h thereafter. A steady state for ion distribution was attained by 4.5 h. Values of mu for H+ and HCO3 minus at 6 h had returned to +0.7 and minus 0.7 mV of control for cisternal CSF and +1.3 and minus 0.6 mV of control for lumbar CSF. The attainment of steady-state values for mu close to control is comparable with passive distribution of these ions between CSF and blood.

Distribution of H+ and HCO3 minus between CSF and blood during metabolic acidosis in dogs

1975 ◽  
Vol 228 (4) ◽  
pp. 1134-1140 ◽  
Author(s):  
EG Pavlin ◽  
TF Hornbein
Keyword(s):  
Metabolic Acidosis ◽  
Extracellular Fluid ◽  
Acid Base Balance ◽  
Ion Distribution ◽  
Acid Base ◽  
Control Series ◽  
Base Balance ◽  
Active Ion Transport ◽  
Arterial Plasma ◽  
Lumbar Cerebrospinal Fluid

To determine whether the regulation of brain extracellular fluid acid-base balance is by active ion transport or passive distribution, changes in cisternal and lumbar cerebrospinal fluid (CSF) (H+) and (HCO3 minus) were assessed in five dogs with normal acid-base status and in six dogs during metabolic acidosis. Both groups were mechanically ventilated to maintain a constant PaCO2. The pH, PCO2, (HCO3 minus), and (lactate) in CSF and arterial plasma and the CSF/plasma DC potential difference were determined at intervals, and the electrochemical potential differnces (mu) for H+ and HCO3 minus were calculated. Following control measurements at pHa equal to 7.40, metabolic acidosis was induced by infusion of 0.6 N HCl. Measurements were made 0, 3, 4.5, and 6 h thereafter and at 0, 3, and 6 h in the control series. A steady state for ion distribution was reached by 4.5 h. In the control series at 6 h the values of mu for H+ and HCO3 minus were within minus 0.2 and +0.5 mV of initial values at the cistern and +0.1 and +0.9 mV at the lumbar site. During metabolic acidosis, the 6-h values at the cistern returned to 0.0 and +0.7 mV of control for muH+ and muHCO3 minus while lumbar values returned to +0.5 and minus 0.4 mV. The closeness of these 6-h values of mu to control is compatible with passive distribution of H+ and HCO3 minus between CSF and blood.

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.

Resistance to Outflow of Cerebrospinal Fluid Determined by Bolus Injection Technique and Constant Rate Steady State Infusion in Humans

Neurosurgery ◽  
1985 ◽  
Vol 16 (3) ◽  
pp. 336-340 ◽  
Author(s):  
Michael Kosteljanetz
Keyword(s):  
Cerebrospinal Fluid ◽  
Steady State ◽  
Bolus Injection ◽  
Point Of View ◽  
Injection Technique ◽  
Communicating Hydrocephalus ◽  
Constant Rate ◽  
High Degree ◽  
Infusion Technique

Abstract Two methods for the determination of resistance to the outflow of cerebrospinal fluid, the bolus injection technique and the constant rate steady state infusion technique, were compared. Thirty-two patients with a variety of intracranial diseases (usually communicating hydrocephalus) were studied. There was a high degree of correlation between the resistance values obtained with the two methods, but values based on the bolus injection technique were systematically and statistically significantly lower than those obtained with the constant rate infusion test. From a practical point of view. both methods were found to be applicable in a clinical setting.

Zidovudine Concentration in Brain Extracellular Fluid Measured by Microdialysis: Steady-State and Transient Results in Rhesus Monkey

2002 ◽  
Vol 301 (3) ◽  
pp. 1003-1011 ◽  
Author(s):  
Elizabeth Fox ◽  
Peter M. Bungay ◽  
John Bacher ◽  
Cynthia L. McCully ◽  
Robert L. Dedrick ◽  
...  
Keyword(s):  
Steady State ◽  
Rhesus Monkey ◽  
Extracellular Fluid ◽  
Brain Extracellular Fluid

scholarly journals The impact of P-gp functionality on non-steady state relationships between CSF and brain extracellular fluid

2013 ◽  
Vol 40 (3) ◽  
pp. 327-342 ◽  
Author(s):  
Joost Westerhout ◽  
Jean Smeets ◽  
Meindert Danhof ◽  
Elizabeth C. M. de Lange
Keyword(s):  
Steady State ◽  
Extracellular Fluid ◽  
Brain Extracellular Fluid ◽  
The Impact

Metabolic alkalosis in models of primary and secondary hyperparathyroid states

1983 ◽  
Vol 245 (4) ◽  
pp. F450-F461 ◽  
Author(s):  
H. N. Hulter ◽  
R. D. Toto ◽  
L. P. Ilnicki ◽  
B. Halloran ◽  
A. Sebastian
Keyword(s):  
Steady State ◽  
Intravenous Infusion ◽  
Metabolic Alkalosis ◽  
Extracellular Fluid ◽  
Chronic Administration ◽  
Systemic Circulation ◽  
Acute Administration ◽  
Group Iii ◽  
Group I ◽  
Renal Origin

Hyperchloremic metabolic acidosis has been reported in clinical states of primary and secondary hyperparathyroidism (HPT). Acute administration of parathyroid hormone (PTH) decreases renal acidification in humans and dogs, but the renal and systemic acid-base effects of chronic HPT have not been extensively investigated. In chronically thyroparathyroidectomized (TPTX) dogs (group I), bPTH 1-5 U/kg twice daily resulted in sustained hypophosphatemia, hypercalcemia, and Cl- -resistant metabolic alkalosis that was of renal origin at least in part: delta [HCO3-]p + 4.1 +/- 0.8 meq/liter, P less than 0.01; delta [H+]p -4 +/- 1 neq/liter, P less than 0.001, days 10-12. The cumulative change (sigma delta) in net acid excretion (NAE) was +44 meq (day 9, P less than 0.05). Similarly, metabolic alkalosis of renal origin, at least in part, occurred when PTH was administered by chronic continuous intravenous infusion (group II). Since chronic administration of calcitriol in dogs results in metabolic alkalosis, plasma calcitriol concentration was measured and found not to be increased by chronic intravenous PTH administration. In intact dogs (group III), a continuous chronic intravenous infusion of the Ca2+ chelator, Na4EGTA (3.0 mmol/kg daily), substituted for an equimolar amount of prechelated EGTA (CaNa2EGTA), resulted in a model of hypocalcemic HPT and severe Cl- -resistant metabolic alkalosis: delta [HCO3-]p +9.1 +/- 1.9 meq/liter, P less than 0.05; delta [H+]p -5 +/- 1 neq/liter, P less than 0.01, days 6-8. NAE decreased significantly. Thus, whereas metabolic alkalosis induced by PTH administration could be accounted for by increased NAE (group I), EGTA-induced metabolic alkalosis was accounted for by an extrarenal mechanism of base input to extracellular fluid (group III). Neutralization of the extrarenal base input by chronic administration of HCl during the period of EGTA-induced HPT did not preclude the development of metabolic alkalosis (group V), suggesting that a renal component was present in EGTA-induced metabolic alkalosis as well as in models of primary HPT (groups I and II). During the steady state, in this group as in the groups administered PTH, the net endogenous load of acid to the systemic circulation requiring renal excretion was unchanged from control, as indicated by stable values of NAE not significantly different from control. Yet metabolic alkalosis persisted in the steady state.(ABSTRACT TRUNCATED AT 400 WORDS)

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