[Renal function in changes in the volume and composition of the extracellular fluid].
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Two biological impedance analyzers, a 50 kHz (RJL) and 20-100 kHz (BMA) instrument, and a total body electrical conductivity (TOBEC) instrument were used to estimate total body water (TBW), extracellular (ECF) and intracellular (ICF) fluid volumes by repeated measurements of 16 normal men (19-38 years old) to assess which, if any, would provide the best estimates. At 3-week intervals, TBW was determined by deuterium dilution, ECF by bromide dilution, ICF by difference (TBW-ECF) and lean body mass by density. Prediction equations were obtained by regression; predicted values for the body fluid volumes were calculated and the results were statistically evaluated. Both the TOBEC and the BMA provided rapid and reliable estimates for body fluid volumes with standard errors of the estimates of about 0.5-1.1 L for ECF, 1.0-1.8 L for TBW, and 1.0-1.3 L for ICF. Part of the error was attributable to standard tracer-dilution methods.
After removal of radioactivity trapped in the extracellular space and correcting for the contribution of connective tissue elements, the K+ -efflux curve of frog sartorius muscles becomes a perfect straight line in a semilogarithmic plot. The simultaneously recorded Na+-efflux curve from the same muscles remains strongly curved, and can be resolved into a slow fraction (which conventionally has been regarded as representing the entire cell Na+) and at least one fast fraction. The fast fraction of Na+ could not have originated from a sarcoplasmic reticulum or any other extracellular space extensions; otherwise a similar fast fraction should exist for K+. The data agree with the interpretation that it is the fast fraction that is rate limiting by cell permeability and the slow fraction by desorption from intracellular adsorption sites.
We have investigated if changes in brain dialysate, reflecting alterations in brain extracellular composition, can be detected during the development of vasogenic brain edema. The blood-brain barrier was opened by intracarotid infusion of 5 or 10 mg protamine sulphate. The rats were killed two hours after opening of the BBB when the brains were macroscopically edematous, after 10 mg but not 5 mg protamine sulphate. No significant alterations in the amino acid concentration in the dialysate were observed after the lower dose. 40 min after infusion of 10 mg protamine, the level of glutamate was significantly increased in the dialysate followed by that of aspartate, glycine, phosphoethanolamine and taurine 10 min later and a further delayed increase in GABA. We conclude that the development of vasogenic brain edema is associated with significant increases in extracellular concentration of excitatory amino acids, of taurine, and of phosphoethanolamine and GABA.
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