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A study of blood-brain barrier in sixteen animals subjected to a variety of experimental conditions, plus clinical studies in three patients, failed to demonstrate the passage of d -tubocurarine from plasma into the cerebrospinal fluid following intravenous or intraarterial injection. A theoretical explanation of this barrier is readily provided in terms of lipid solubility and dissociation constant for d -tubocurarine.

The distribution and elimination of d -tubocurarine were investigated in 30 dogs at a minimal paralyzing dose and at a second higher concentration sufficient to produce saturation of depots. The concentration of d -tubocurarine in the muscle tissue closely paralleled that found in the plasma. At lower dose levels, the liver played little role in the distribution of d -tubocurarine, but with larger dosage the liver served as an important reservoir. The nephrectomized animal appeared to be able to reduce plasma concentrations of d-tubocurarine although the second phase of redistribution was slowed or eliminated. An additional study was undertaken to evaluate the protein binding of d-tubocurarine, and this was found to occur with each of the protein fractions examined. Data from these studies were analyzed with the help of a multicompartment analog model.