Electrolyte- and fluid-spaces of rat brain in situ after infusion with dinitrophenol.
Chemical distribution measurements of radioactive sodium-thiosulfate (35S) and of the brain water indicate that infusion of 2.4-dinitrophenol into  a carotid artery of rats caused a water uptake and fluid shifts from the extra- into the intracellular compartments in the central nervous system. The extracellular marker compound was administered to the brain via ventriculo-cisternal perfusion and intravenous injection yielding almost equal concentrations in plasma-water and perfusate. In order to prevent an active efflux of the label from the tissue, high concentrations were utilized in the perfusate to saturate potential outward transport mechanisms. The indicator space (based on total brain water) was 16% in controls and 12% in experimental animals when marker equilibrium had been attained, which is equivalent in reduction of the extracellular space of about 1/4. Intracellular water and Na+ rose after DNP, while K+ remained all but unchanged. The fluid shift into the intracellular compartment was found to relate closely with a cellular uptake of Na+. The Na+ concentration both in plasma and in the perfusion fluid leaving the ventricular system was consistently reduced in experimental animals. The K+ concentration was significantly elevated in the plasma of experimental animals but virtually unchanged in the cisternal effluate.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D004140:Dinitrophenols / Q000494:pharmacology*; D007424:Intracellular Fluid / Q000378:metabolism; D008297:Male; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013997:Time Factors; D014882:Water-Electrolyte Balance / Q000187:drug effects*
D004140:Dinitrophenols; D012964:Sodium; D011188:Potassium