The Iodide Space in Rabbit Brain

Citation

Ahmed, Nawal Abd El-Hay (1968) The Iodide Space in Rabbit Brain. Dissertation (Ph.D.), California Institute of Technology. doi:10.7907/E49K-K156. https://resolver.caltech.edu/CaltechTHESIS:08302016-104724672

Abstract

In the present investigation labeled iodide was used to investigate the interrelationship between brain, blood and cerebrospinal fluid, to examine active transport across the blood-brain- and the blood-cerebrospinal fluid barriers, and to estimate the extracellular space of the brain.

The iodide space in the brain and the iodide concentration in cerebrospinal fluid after intravenous administration of radioactive iodide are determined by the following mechanisms. Iodide passes into the cerebrospinal fluid but active transport in the choroid plexus moves most of the iodide back again into the plasma, keeping the concentration at a very law value. An extracellular fluid is formed at the blood-brain barrier possibly in a similar way. The iodide concentration of this fluid is unknown but is probably higher than that in the cerebrospinal fluid. Diffusion of iodide across the brain-cerebrospinal fluid barrier transports this ion from the brain into the cerebrospinal fluid which is constantly renewed "sink action".

The iodide space was found to be 2.4% four to five hours after the intravenous administration of ¹³¹I, the iodide content of the cerebrospinal fluid was 1.2% of that of the TCA serum filtrate. The iodide space increased to 10.6% in preparations in which in addition to ¹³¹I unlabeled iodide (to a serum concentration of 25 to 50 mM) was administered to saturate the active transport processes in the choroid plexuses and blood-brain barrier. The iodide activity of the cerebrospinal fluid in these experiments increased to 29.3% of that in the TCA serum filtrate. In experiments in which the inhibitor of iodide transport, perchlorate (8 mM), was injected intravenously with the ¹³¹I-, the iodide space was 8.2% and the iodide concentration in the cerebrospinal fluid 26.4%. These experiments demonstrate the effect of saturation and inhibition of active transport on the iodide space. They show furthermore that the depression of the active transport did not raise the iodide concentration in the cerebrospinal fluid to the plasma concentration. The relatively low (1/3 of that in the serum TCA filtrate) iodide concentration in the cerebrospinal fluid under these circumstances was ascribed to a differential permeability of the blood-cerebrospinal fluid barrier for iodide and chloride.

The sink action can be eliminated by perfusion of the ventricles with an artificial cerebrospinal fluid containing iodide. Ventriculocisternal perfusion with ¹³¹I- alone resulted in an iodide space of 7.2% after 4.5 hours. An iodide space of 10.2% was determined by a combined intravenous administration and ventricular perfusion with an artificial cerebrospinal fluid containing the same concentration of ¹³¹I as present in the plasma. When in similar experiments perchlorate was administered intravenously, the iodide space rose to 16.8%. The iodide space determined by simultaneous intravenous injection and ventricular perfusion with both labeled and unlabeled iodide, in a concentration sufficient to saturate the active transport, was 20.8%. In the latter instances the sink action is eliminated and also active transport is inhibited or saturated. It was postulated that under these conditions the iodide concentration in plasma and brain extracellular fluid are approximately the same. The use of the iodide space as a measure of the brain extracellular space was discussed.

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