A gel partition model for organic desorption from a pond sediment.

Adsorption at the water-sediment interface has been correlated with the organic carbon content of natural sediment samples and with water-octanol partitioning equilibria. In deriving a new model for sorption in sediment, it is assumed that adsorption is due to humin-kerogen polymers associated with the clay component in the sediment. The model includes solubility parameter theory applied to solute-gel-liquid interactions and a theory of the liquid-polymer interactions that control gel swelling. Partially swollen gels are expected to exhibit impeded diffusion. These concepts are able to explain observations of limited desorption of certain organic compounds from natural sediments and soil minerals. Experiments were performed in which extractive solvents flowed through a liquid chromatographic column packed with dried estuarine and pond sediment samples and the effluent was analyzed for a test lipophilic compound, di(2-ethylhexyl) phthalate. The model predicts that the maximum desorption rate and the maximum extent of gel swelling should coincide and, conversely, that the desorption rate should be diffusion-limited if the polymer gel is only partially swollen. The conditions for maximum desorption and for diffusion-limited desorption were both observed experimentally.

Cocaine and D-amphetamine induce changes in central beta-adrenoceptor sensitivity: effects of acute and chronic drug treatment.

The effects of acute and chronic treatment with psychomotor stimulants on specific binding of [3H]dihydroalprenolol to beta-adrenoceptors in rat brain were examined. At a dose of 10 mg/kg both acute and chronic treatment with cocaine and chronic treatment with D-amphetamine (10 mg/kg) caused increased binding of [3H]dihydroalprenolol. The molecular mechanism for this enhanced binding appears to be augmentation of the density of beta-adrenoceptors in rat brain. At a lower dose (5 mg/kg), however, chronic administration of D-amphetamine caused a decrease in the density of beta-adrenoceptors in rat brain. Chronic treatment with either D-amphetamine (10 mg/kg) or cocaine induced a marked increase in the magnitude of cyclic AMP accumulation in rat brain slices elicited by norepinephrine. Acute as well as chronic administration of D-amphetamine in vivo inhibited the temperature-dependent uptake of [3H]norepinephrine in rat brain synaptosomal homogenates, but no such inhibition was observed after chronic or acute treatment with cocaine. The results suggest that psychomotor stimulants induce beta-adrenoceptor supersensitivity which may be involved in the phenomenon of reverse tolerance and possibly psychosis in humans. The development of beta-adrenoceptor supersensitivity does not appear to be mediated through alterations in norepinephrine transport at the presynaptic sites.