Na, K, Ca, Mg, AND Cl CONCENTRATIONS IN CHOROID PLEXUS FLUID AND CISTERNAL FLUID COMPARED WITH PLASMA ULTRAFILTRATE

SUMMARY1. A method was developed for isolating a segment of the choroid plexus of the lateral ventricle of the cat brain in a chamber in situ.2. A comparison of electrolyte and protein concentrations in serum, ultrafiltrate of serum, cisterna magna fluid, fluid accumulated in the chamber and fluid collected from the choroid plexus by another technique, demonstrates that the chamber fluid is a secretary product of the choroid plexus.3. The rate of fluid formation in the chamber was 0 4 10. min-mg-' of tissue, a value in good agreement with reports in the literature.4. The observation that the concentration of K+ in choroid plexus fluid was lower than that in the serum ultrafiltrate suggests that K+ is regulated by an active transport process at the choroid plexus.5. Significant correlation was found between electrolyte values and the protein content of the chamber fluid. This suggests that plasma is the probable source of the protein in the chamber fluid and that K+ and probably Ca2+ and Mg2+ in c.s.f. are subject to active homoeostatic regulation by the choroid plexus. 6. The technique described provides a new opportunity to study in detail the functional characteristics of the choroid plexus.

Section: Electrolyte Concentrationssupporting

confidence: 90%

Composition of fluid obtained from choroid plexus tissue isolated in a chamber *in situ**

Miner¹,

Reed²

1972

“…A similar gradient between c.s.f. and plasma has been reported by Ames, Sakanoue &Endo, 1964 andCserr, 1975. It is shown in Fig. 2 that sodium entry from blood into c.s.f., when high-potassium artificial c.s.f.…”

Section: Discussionmentioning

confidence: 78%

The effect of lithium on electrolyte transport by the in situ choroid plexus of the cat.

Reed¹,

Yen²

1980

SUMMARY1. The effects of lithium on electrolyte transport were studied by using the cat choroid plexus isolated in a chamber in situ.2. Lithium infused intravenously to produce plasma lithium concentrations up to 5 m-equiv/l. caused an increase in plasma magnesium with no effect on the concentration of magnesium in the chamber fluid.3. When 22NaCl was infused intravenously the chamber fluid/plasma ratio of 22Na was nearly 1 in the first 30 min sample and at the steady state it was significantly greater than 1.4. When lithium chloride (1-5 m-equiv/l.) or potassium chloride (6.6 m-equiv/l.) was added to the chamber at the start of a collection period with plasma 22Na in the steady state, the 22Na content of the chamber fluid promptly increased 118 and 68 %, respectively, above the control value with no increase in secretary rate.5. The addition of ouabain to the chamber fluid, in addition to the lithium chloride or potassium chloride, tended to stimulate or have no significant effect on 22Na uptake at a concentration of 10-5 M and to reduce it as well as the secretary rate at 10-3 M.6. The data are compatible with there being two functionally separate sodium transport systems in the choroid plexus. One transports sodium accompanied by an anion and water to provide the fluid secreted into the chamber (c.s.f.) and the other operates primarily to regulate the potassium concentration of the c.s.f. by pumping potassium out in exchange for sodium.7. Lithium can be transported by both systems to a limited extent and the presence of lithium in the c.s.f. stimulates the sodium-potassium regulating pump.

“…greater than that of large cavity c.s.f. (Ames, Sakanoue & Endo, 1964;Miner & Reed, 1972). Analysis of data on the kinetics of labelled bicarbonate movement from blood to c.s.f.…”

Section: Discussionmentioning

confidence: 99%

Regulation of cerebrospinal fluid bicarbonate by the cat choroid plexus.

Husted¹,

Reed²

1977

1. The regulation of cerebrospinal fluid (c.s.f.) bicarbonate concentration was studied using the cat choroid plexus isolated in a chamber in situ. 2. Decreases in plasma bicarbonate concentration caused relatively small changes in the c.s.f. bicarbonate concentration. 3. Alterations in c.s.f. bicarbonate concentration (c.s.f. HCO3‐=9 or 28 m‐equiv/l.) were countered by changes in the bicarbonate concentration of the fluid produced by the plexus or in the rate of bicarbonate transport which returned c.s.f. bicarbonate towards normal. 4. There was significant regulation of pH in the choroid plexus fluid during hypocapnia and hypercapnia. 5. Alterations of plasma acid‐base status did not significantly alter the potential difference across the choroid plexus. However, the potential difference increased when c.s.f. bicarbonate was increased and decreased when c.s.f. bicarbonate was decreased. 6. The data indicate that the bicarbonate concentration in the c.s.f. is actively regulated by the choroid plexus during acid‐base disturbances occurring either systemically or in the c.s.f.