Effects of inhibitors on chloride outflux from cerebrospinal fluid

1988 ◽  
Vol 64 (5) ◽  
pp. 2183-2189 ◽  
Author(s):  
M. Nishimura ◽  
D. C. Johnson ◽  
H. Kazemi
Keyword(s):  
Cerebrospinal Fluid ◽  
State Level ◽  
Compartment Model ◽  
Disulfonic Acid ◽  
Acid Base Balance ◽  
Quantitative Measurements ◽  
Ventriculocisternal Perfusion ◽  
Base Balance ◽  
Anesthetized Dogs ◽  
The Difference

Movement of chloride from cerebrospinal fluid (CSF) to brain or blood is one of the factors that may be involved in regulation of CSF [Cl-], which is important to CSF acid-base balance. We made quantitative measurements of the unidirectional outflux of radiolabeled chloride (38Cl, half-life 37.3 min) from CSF in anesthetized dogs, using ventriculocisternal perfusion (VCP). The outflux of 38Cl from CSF was determined from the difference between the movements of 38Cl and dextran using a one-compartment model. VCP was performed at a rate of 1.4 ml/min for 14 min, and then slowed to 0.28 ml/min. The 38Cl activity decreased to a steady-state level approximately 12% lower than that of dextran within 40–50 min. Under control conditions for the first run (n = 24), the flux was 0.042 +/- 0.003 (SE) ml/min. The outflux under control conditions (n = 6) tended to increase over three separate determinations in a 6-h period, being 136 +/- 19% of the first run on the second run, and 143 +/- 24% on the third. There were no significant changes in 38Cl outflux compared with control ratios after the inclusion of bumetanide in the VCP fluid (n = 6), which inhibits sodium-coupled Cl- transport, with acetazolamide (n = 6), which inhibits carbonic anhydrase, or with 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (n = 6), an inhibitor of carrier-mediated anion exchange. These results suggest that the outward movement of chloride from CSF occurs mostly by passive diffusion and is not by mediated transport.

Chloride flux from blood to CSF: inhibition by furosemide and bumetanide

1987 ◽  
Vol 63 (4) ◽  
pp. 1591-1600 ◽  
Author(s):  
D. C. Johnson ◽  
S. Singer ◽  
B. Hoop ◽  
H. Kazemi
Keyword(s):  
Chloride Transport ◽  
Extracellular Fluid ◽  
Compartment Model ◽  
Acid Base Balance ◽  
Major Mechanism ◽  
Quantitative Measurements ◽  
Ventriculocisternal Perfusion ◽  
Base Balance ◽  
Anesthetized Dogs ◽  
Three Compartment Model

Movement of chloride from blood to cerebrospinal fluid (CSF) is one of the factors that may be involved in regulation of CSF [Cl-], which is important to CSF acid-base balance. We made quantitative measurements of the unidirectional flux of radiolabeled chloride between blood and CSF in anesthetized dogs, using 38Cl, a short-lived isotope (half-life 37.3 min). This allowed multiple studies to be performed in a given animal. A three-compartment model for the blood, CSF, brain extracellular fluid, and ventriculocisternal perfusion system was used to determine the flux rate. With normocapnia, the flux was 0.01.1 min-1. The influx could be reproducibly measured for three separate determinations in the same animal over a period of 6 h, being 98 +/- 6% of the control first run on the second run and 113 +/- 6% on the third. Furosemide and bumetanide, inhibitors of sodium-coupled chloride movement, lowered the flux to 43 +/- 3% and 55 +/- 6% of control, respectively. The combination of hypercapnia and furosemide lowered the influx to 63 +/- 9% of control. These results indicate that a major mechanism of chloride entry into CSF is sodium-dcoupled chloride transport.

Acid-Base Balance in Cerebrospinal Fluid

1965 ◽  
Vol 12 (5) ◽  
pp. 479-496 ◽  
Author(s):  
J. B. POSNER ◽  
A. G. SWANSON ◽  
F. PLUM
Keyword(s):  
Cerebrospinal Fluid ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Afferent vagal stimulation, vasopressin, and nitroprusside alter cerebrospinal fluid kinin

1987 ◽  
Vol 253 (1) ◽  
pp. R136-R141 ◽  
Author(s):  
G. R. Thomas ◽  
H. Thibodeaux ◽  
H. S. Margolius ◽  
J. G. Webb ◽  
P. J. Privitera
Keyword(s):  
Cerebrospinal Fluid ◽  
Vagal Stimulation ◽  
Cardiovascular Regulation ◽  
Perfusion System ◽  
Ventriculocisternal Perfusion ◽  
Anesthetized Dogs ◽  
Bilateral Vagotomy ◽  
Afferent Vagal ◽  
Nitroprusside Infusion ◽  
Stimulation Of

The effects of afferent vagal stimulation, cerebroventricular vasopressin, and intravenous nitroprusside on cerebrospinal fluid (CSF) kinin levels, mean arterial pressure (MAP), and heart rate (HR) were determined in anesthetized dogs in which a ventriculocisternal perfusion system (VP) was established. Following bilateral vagotomy, stimulation of the central ends of both vagi for 60 min significantly increased MAP and CSF perfusate levels of kinin and norepinephrine (NE). MAP was increased a maximum of 32 +/- 4 mmHg, and the rates of kinin and NE appearance into the CSF perfusate increased from 4.2 +/- 1.4 to 22.1 +/- 6.9 and from 28 +/- 5 to 256 +/- 39 pg/min, respectively. A significant correlation was found between CSF kinin and NE levels in these experiments. In other experiments the addition of arginine vasopressin to the VP system caused a significant increase in CSF perfusate kinin without affecting MAP or HR. Intravenous infusion of nitroprusside lowered MAP without affecting kinin levels in the CSF. However, on cessation of nitroprusside infusion, CSF kinin increased significantly in association with the return in MAP to predrug level. Collectively the data are consistent with the hypothesis that central nervous system kinins have some role in cardiovascular regulation, and furthermore that this role may involve an interaction between brain kinin and central noradrenergic neuronal pathways.

Influence of bafilomycin A1on pHi responses in cultured rabbit nonpigmented ciliary epithelium

1997 ◽  
Vol 273 (5) ◽  
pp. C1700-C1706 ◽  
Author(s):  
Qiang Wu ◽  
Nicholas A. Delamere
Keyword(s):  
Plasma Membrane ◽  
Disulfonic Acid ◽  
Ciliary Epithelium ◽  
Free Medium ◽  
Acid Base Balance ◽  
Carbonyl Cyanide ◽  
Base Balance ◽  
Rich Solution ◽  
Cytoplasmic Acidification ◽  
Nonpigmented Ciliary Epithelium

Aqueous humor secretion is in part linked to [Formula: see text]transport by nonpigmented ciliary epithelium (NPE) cells. During this process, the cells must maintain stable cytoplasmic pH (pHi). Because a recent report suggests that NPE cells have a plasma membrane-localized vacuolar H+-ATPase, the present study was conducted to examine whether vacuolar H+-ATPase contributes to pHi regulation in a rabbit NPE cell line. Western blot confirmed vacuolar H+-ATPase expression as judged by H+-ATPase 31-kDa immunoreactive polypeptide in both cultured NPE and native ciliary epithelium. pHi was measured using 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Exposing cultured NPE to K+-rich solution caused a pHi increase we interpret as depolarization-induced alkalinization. Alkalinization was also caused by ouabain or BaCl2. Bafilomycin A1 (0.1 μM; an inhibitor of vacuolar H+-ATPase) inhibited the pHi increase caused by high K+. The pHi increase was also inhibited by angiotensin II and the metabolic uncoupler carbonyl cyanide m-chlorophenylhydazone but not by ZnCl2, 4-acetamido-4′-isothiocyanostilbene-2,2′-disulfonic acid (SITS), 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS), omeprazole, low-Cl−medium, [Formula: see text]-free medium, or Na+-free medium. Bafilomycin A1 slowed the pHi increase after an NH4Cl (10 mM) prepulse. However, no detectable pHi change was observed in cells exposed to bafilomycin A1 under control conditions. These studies suggest that vacuolar H+-ATPase is activated by cytoplasmic acidification and by reduction of the proton electrochemical gradient across the plasma membrane. We speculate that the mechanism might contribute to maintenance of acid-base balance in NPE.

scholarly journals Acid base balance in blood and cerebrospinal fluid.

1985 ◽  
Vol 60 (6) ◽  
pp. 579-581 ◽  
Author(s):  
Y Horovitz ◽  
I Tal ◽  
A Keynan
Keyword(s):  
Cerebrospinal Fluid ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Potassium exchange between cerebrospinal fluid, plasma, and brain

1965 ◽  
Vol 209 (6) ◽  
pp. 1219-1226 ◽  
Author(s):  
Helen Cserr
Keyword(s):  
Cerebrospinal Fluid ◽  
Specific Activity ◽  
Potassium Concentration ◽  
Extracellular Fluid ◽  
Ionic Fluxes ◽  
Ventriculocisternal Perfusion ◽  
Anesthetized Dogs ◽  
The Relationship ◽  
Potassium Exchange ◽  
Total Potassium

Potassium exchange between cerebrospinal fluid (CSF), plasma, and brain was investigated in anesthetized dogs and rats using the technique of ventriculocisternal perfusion. Transport via bulk secretion and absorption of CSF accounts for only 20% of total potassium exchange, unidirectional ionic fluxes across the ependyma for 80%. This large transependymal exchange is primarily between CSF and brain intracellular potassium pools, since two-thirds of the K42 outflux can be recovered from brain tissue. Conversely, much of transependymal influx comes from brain, as demonstrated by the low specific activity of influx relative to that of plasma following intravenous injection of K42. Potassium outflux is almost proportional to CSF [K+] in the range 0–10 mEq/liter but is independent of plasma [K+]. Perfusion with 10–5 m ouabain reduces transependymal K42 outflux to 25% of control; the residual outflux may be accounted for by passive processes. Results are discussed in terms of 1) regulation of CSF potassium concentration and 2) the relationship between CSF and brain extracellular fluid.

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