Abstract

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.