Acid-Base Status and Gases in Cerebrospinal Fluid of Healthy Calves and Buffalo Calves

2010 ◽  
Vol 28 (2) ◽  
pp. 131-134 ◽  
Author(s):  
Jit Singh ◽  
Kuldip K. Mirakhur ◽  
B. Prasad ◽  
R. N. Kohli
Keyword(s):  
Cerebrospinal Fluid ◽  
Buffalo Calves ◽  
Acid Base ◽  
Acid Base Status

Sodium, chloride, and bicarbonate movement from plasma to cerebrospinal fluid in cats

1975 ◽  
Vol 228 (3) ◽  
pp. 673-683 ◽  
Author(s):  
BP Vogh ◽  
TH Maren
Keyword(s):  
Cerebrospinal Fluid ◽  
Carbonic Anhydrase ◽  
Choroid Plexus ◽  
Rate Constants ◽  
Secretory Cells ◽  
Acid Base ◽  
Rapid Exchange ◽  
Primary Signal ◽  
Carbonic Anhydrase Inhibition ◽  
Acid Base Status

Rate constants have been determined for the entry of 22Na+, 36Cl minus, and H14CO3- into CSF from plasma in cats during changes in Pco2 with and without inhibition of carbonic anhydrase. The application of these rate constants to movement of unlabeled electrolytes suggests that Na+ and Cl minus enter CSF by a one-way flux into newly formed fluid, but that entering HCO3-is involved both in net accumulation in new fluid and in rapid exchange with existing HCO3-. The entering HCO3-ions are not transferred from plasma but are formed in secretory cells from dissolved CO2. The exchange component of HCO3-entry is Pco2-dependent; entry of Na+ and Cl minus is not; hence net rate of HCO3-formation estimated by difference between Na+ and Cl minus is not Pco2 dependent. The net rate of HCO3-formation lies within the availability of CO2 from blood flow to choroid plexus but is not necessarily limited to this tissue. When carbonic anhydrase is inhibited, the net rate of formation of HCO3-is close to the calculated uncatalyzed rate expected for choroid plexus. The entry of all three ions is reduced by carbonic anhydrase inhibition, but the enzyme does not seem to provide the primary signal for alteration of CSF acid-base status. Regulation of CSF pH appears to be achieved through changes in HCO3-concentration that occur subsequent to the secretion of HCO3--rich new fluid.

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-].

Central chemical control of ventilation and response of turtles to inspired CO2

1985 ◽  
Vol 249 (3) ◽  
pp. R323-R328 ◽  
Author(s):  
B. M. Hitzig ◽  
J. C. Allen ◽  
D. C. Jackson
Keyword(s):  
Cerebrospinal Fluid ◽  
Tidal Volume ◽  
Chemical Control ◽  
Ventilatory Response ◽  
Freshwater Turtles ◽  
Acid Base ◽  
Ventilatory Responses ◽  
Acid Base Status ◽  
Homeostatic Mechanisms

The role of central chemosensors in the overall ventilatory response of freshwater turtles (Chrysemys scripta elegans) to the addition of CO2 in inspired gas was measured. Centrally mediated ventilatory responses were isolated in the unanesthetized animal by combining CO2 breathing and brain ventricular perfusion with mock cerebrospinal fluid (CSF) of varying acid-base status. Breathing 4.5% CO2 resulted in increases in both ventilatory frequency (f) and tidal volume (VT), with increases in VT providing most of the overall ventilatory change. Alterations in the acid-base status of the perfusate produced highly significant changes in f. VT changes were divorced from the acid-base status of the mock CSF perfusate. We therefore conclude that ventilatory changes in turtles, mediated by central chemosensors, are primarily affected by alterations in f. VT changes, associated with acid-base homeostatic mechanisms, are mediated by receptors outside the blood-brain barrier in these animals. On the basis of these data, we hypothesize that the increase in f observed when turtles breathe 4.5% CO2 is primarily mediated by the central chemosensors.

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