Alkylated polymer surface, buffering

Alkyl monoesters of poly(vinyl methyl ether-maleic anhydride) (PVM-MA) are bioerodible acidic polymers that are used to control drug release. In biological fluids with poor buffering capacity, drug release from the polymers and their dissolution are slowed owing to the lower pH on the polymer surface. We studied whether the release of timolol from matrices of monoisopropyl ester of PVM-MA in vitro and in vivo in rabbits eyes could be affected by disodium phosphate in the matrices. Addition of disodium phosphate to the matrices doubled the release rate of timolol in vitro, but it did not affect the bulk pH of the dissolution medium. On the basis of the timolol concentrations in the tear fluid and in systemic circulation, disodium phosphate seems to accelerate drug release in vivo also. Disodium phosphate probably affects the rate of dmg release by increasing the microenvironmental pH on the polymer surface. 

Vezin and Florence (1980) used monodisperse powdered polymer particles for studying the in vitro degradation of poly(7j-alkyl a-cyanoacrylates), with a range of alkyl side chains and MW. These authors showed that degradation in aqueous buffer depends not only upon the pH and the length of the polymer alkyl side chain, but also critically on the polymer particle surface, particle size, polyoner MW and MW distribution. They concluded that at low MW (below the characteristics of effective tissue adhesiveness), increased water solubility, plasticity and diffusivity may result in a bulk rather than surface polymier degradation. 

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