1. The raffinose space, the inulin space and the weight loss on compression of perfused rat hearts are indistinguishable in magnitude.2. The inulin space shows systematic variations from day to day and is also affected by the procedure used for removing surplus water from the perfused heart. It is therefore not safe to use a mean figure of extracellular space in permeability experiments.3. Perfusion of hearts with arabinose solutions alters the intracellular water content. These alterations can be accounted for if it is assumed that the arabinose which penetrates the cells is uniformly distributed in the cell water.4. By appropriate choice of pentose concentration and of time of perfusion it can be shown that all the estimated cell water is accessible to pentose.5. It is concluded that no detectable fraction of the extracellular water is inaccessible to inulin and that no detectable fraction of the intracellular water is inaccessible to pentose.

Animals↗

PubMed1970

Kinetics of pentose permeation in the perfused rat heart.

1. The fractional permeation of heart cell water by L-arabinose and D-xylose after a standard period of perfusion is less the higher the extracellular pentose concentration.2. At any given pentose concentration the kinetics of permeation are consistent with passive diffusion through the cytoplasm or with transport across the cell membrane by a saturable carrier.3. The concentration dependence of permeation is inconsistent with passive diffusion.4. The kinetics of L-arabinose permeation are consistent with a carrier having V(max) = 2.2 m-mole/l. extracellular water per min and a half-saturation concentration [K] of 0.5 x 10(-4)M. The corresponding figures for D-xylose are V(max) = 1.4, [K] = 1.6 x 10(-4)M.

Animals↗

PubMed1970

The effect of insulin on the kinetics of pentose permeation of the rat heart.

1. The kinetics of permeation of pentoses into the rat heart in the presence of insulin are similar in nature to those in the absence of insulin.2. The half-saturation concentration of the carrier system is increased by insulin in a manner which is independent of insulin concentration.3. The V(max) of the carrier system is altered by insulin in a graded fashion: at low insulin concentrations it may be lower than in the absence of insulin.4. It is shown that these effects can be accounted for if insulin combines with the carrier and thereby increases either the rate constant governing the mobility of the carrier in the membrane or the rate constant governing dissociation of the sugar-carrier complex.5. The effects cannot be accounted for by a graded action of insulin on the membrane as distinct from the carrier.

Animals↗