Factors Influencing the Exchange of Sodium Between Plasma and Cerebrospinal Fluid*†

Abstract

This study is concerned with the mechanism of exchange of sodium between plasma and cerebrospinal fluid (CSF). Several workers (1, 2) have reported that there is no significant difference between the concentration of sodium in plasma and CSF. reported that the average concentration of sodium in CSF, in man, exceeded the plasma concentration by about four mEq. Davson (4) has determined the distribution ratio of sodium between CSF and plasma as 0.975 in the dog, correcting for the difference in water content of these fluids. Despite the similarity in sodium concentration of these fluids and the superficial resemblance of CSF to a protein-free filtrate of plasma, intravenously administered radio-sodium reaches equilibrium in the CSF far more slowly than in the extracellular fluid (5, 6). The delay in exchange between plasma and CSF has been attributed to the existence of a blood-CSF barrier for sodium (5-7). The present experiments have been devised to note the effect of a variety of physiological and pharmacological alterations on the exchange of sodium between these fluid compartments. intervals. The time necessary for the activity of the cisternal fluid to reach 50 per cent of the serum activity was obtained by graphic analysis of the CSF/serum ratios at these time intervals. As the serum radioactivity was not maintained at a constant level, a time constant was not calculated but the half-time as determined was used as the measure of the rate of sodium exchange. This half-time is referred to as the sodium exchange time. A typical experiment is illustrated in Figure 1. Radioactivity was measured in duplicate with a welltype scintillation counter and sodium content with a flame photometer. Each animal had at least one control study in addition to one or more experimental studies. Each animal was given at least a seven day recovery period between experiments. Cisternal fluid pressure, when required, was measured with a spinal water manometer. Blood pressure was recorded in some experiments with a strain-gage manometer. METHODS RESULTSI. Concentration of sodium in serum and cerebrospinal fluid of normal dogs The serum and CSF sodium concentrations were determined in 27 normal dogs. The average serum sodium concentration was 155 ± 6 mEq. per L. The average CSF sodium concentration was 158 + 6 mEq. per L. Statistical analysis using Student's "t" test (8)

Cortical pH and the blood‐brain barrier

“…The resistance of the acidic response to 10 % (v/v) C02 agrees with the barrier resistance to trypan blue (Clemedson, Hartelius & Holmberg, 1958), to 24Na (Fishman, 1959), and to albumin (Lending et al 1961). …”

Arginine vasopressin V1-antagonist and atrial natriuretic peptide reduce hemorrhagic brain edema in rats.

“…Intravenous injection of AVP enhanced sodium transport into the cerebrospinal fluid (CSF) and lowered CSF production. 1 -2 Intraventricular injection of AVP increased transport of labeled water from blood to brain, enhanced water movement across the arachnoid villi, increased brain water content, aggravated cold-injury edema, and increased ependymal permeability but did not alter CSF production. 3 -7 In an earlier study we showed that the intracerebral injection of AVP caused an increase in brain water content that could be inhibited by an antagonist to the V, receptor of vasopressin.…”

The Cerebrospinal Fluid as a Pathway in Neuroendocrine Integration

“…The gall bladder is another example in which sodium is pumped from epithelial cells into intercellular channels, which are distended when sodium transport is acceler¬ ated and collapsed when sodium transport is inhibited (Tormey & Diamond, 1967). Fishman (1959) also obtained experimental evidence suggesting that the choroid plexusses were a target for the action of ADH in enhancing the exchange of sodium between plasma and CSF. Leusen & Lacroix (1961) found that the intraventricular infusion of hypotonie saline had a diuretic effect, perhaps because the decrease of sodium concentration in the CSF reduced or stopped the release of ADH from the neural lobe.…”