Magnesium exchange between plasma and cerebrospinal fluid (CSF) was studied in dogs using Mg28Cl2 and MgCl2. Normal CSF/plasma magnesium ratio in this animal is 1.34. In face of a plasma magnesium concentration 300–400% of normal, the CSF magnesium only rose to a maximum of 21% above control at the end of 5.5 hr. Intravenously injected Mg28Cl2 enters the CSF rapidly, reaching equilibrium within 2–3 hr. The exit rate of magnesium from the CSF has a half time of about 70 min when CSF magnesium levels are close to normal or they are greatly elevated. This rate is not affected by increasing plasma magnesium concentrations. It is concluded that an active transport mechanism is involved in transporting magnesium from blood to CSF, and that diffusion and bulk filtration are responsible for the removal from the CSF.
Digitalis-sensitive Na-K activated ATPase (Na-K ATPase), implicated in active cation transport, was shown to occur in cat choroid plexus. Cerebrospinal fluid (CSF) formation rate, measured by collection from cat cerebral aqueduct was inhibited 18% by intravenous desacetyl lanatoside C (0.2 mg/kg). Ouabain, placed intraventricularly, caused inhibition of flow, ranging from 100% by 10–5 mole to 0% by 5 x 10–10 mole. After 10–6 mole ouabain, Na-K ATPase activity in lateral ventricle choroid plexus was inhibited 69% without change in digitalis-insensitive, Mg activated ATPase and carbonic anhydrase activities. Ventriculocisternal perfusion with varying concentrations of ouabain, scillaren A, and hexahydroscillaren A gave CSF flow inhibition (inulin dilution technique) correlating quantitatively with in vitro Na-K ATPase inhibition. Other compounds studied were erythrophleine, cassaine, and l-norepinephrine. It is concluded that the choroid plexus Na-K ATPase system has a primary function in the formation of CSF in the cat, presumably through the active secretion of Na ions into the ventricle.
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