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• W2765865587 abstract "Application of the method of electrically facilitated ion transport across biologicalnmembranes (iontophoresis) has been successful in the treatment of neurogenic pain statesn(Csillik et al, 1982). Such pain states include post-herpetic neuralgia, painful diabeticnneuropathy, chronic regional pain syndromes and phantom pain. The main agents used innthese studies are the vinca alkaloids including vincristine and vinblastine. It has beennsuggested that the vinca alkaloids cause remittance of neurogenic pain via blockade ofnmicrotubules in the neuron. Microtubules are involved with the movement of importantnchemical transmitters within the neuron such as nerve growth factor, which has beennimplicated in the development and maintenance of neurogenic pain. The method used bynCsillik et al (1982), in the iontophoretic delivery of vinca alkaloids was not theoreticallynoptimal. It was therefore desirable to gain an understanding of vinca alkaloidniontophoresis in order to further understand the mechanism of action of pain relief.nConsidering vinca alkaloids have considerable molecular weights (approximately 850nDa) and that molecular weight is considered a factor in achieving appreciablentransepidermal iontophoretic flux, the possibility of developing a predictive algorithm fornflux based on molecular weight was investigated.nAn investigation into the causative aspect of neurogenic pain symptoms in the animalnmodel described by Bennett and Xie (1988) was undertaken. In vitro and in vivontransdermal penetration studies utilizing various methods of iontophoresis werenundertaken. An optimal method was determined. This method was applied to the chronicnconstriction injury rat pain model in a controlled manner in order to quantify thenoutcome. In vivo permeation studies involving iontophoresis of a group of compoundsnwith a broad molecular weight range was undertaken. This data was pooled withnliterature data in an attempt to mathematically describe the effect of molecular weight onnthe iontophoretic permeability co- efficient.Investigation of axoplasmic transport in the Bennett and Xie (1988) model of neurogenicnpain indicated an increase in the amount of material being transported along the nerve innthe retrograde direction. In vitro studies determined that the optimum conditions fornvincristine iontophoresis may include a donor vehicle of HEPES buffer of approximatenpH 6.2.In vitro and in vivo studies indicated that iontophoresis of vincristine resulted innappreciable levels in the nerve without significant systemic distribution. Neuronal levelsnwere sufficient to inhibit axoplasmic transport. When applied to the pain model, thenmethod did not affect pain scores. Analysis of in vitro iontophoretic flux data pooled withnliterature data indicated that molecules of molecular weight between 500 and 6000 Danhad similar fluxes. The logarithm of the iontophoretic permeability co-efficient ofnpermeants between atomic weight 22 Da and molecular weight 500 Da, demonstrated annexponential decay profile.nResults indicated that vincristine iontophoresis was not likely to have caused the positiveneffect on pain scores reported by Csillik et al (1982). Data also indicated thatnmanipulation of the donor vehicle could positively effect the transepidermal iontophoreticnpenetration of vincristine compared to the method used by Csillik et al (1982). Increasednvincristine flux did not result in reduction of pain scores in the Bennett and Xie (1988)nmodel of neurogenic pain. There was however, an appreciable increase in material beingntransported retrogradely in nervous tissue of the affected paw in the rat.nWhere maximal drug fluxes are desirable, ideal drug candidates for transepidermalniontophoresis would have atomic/molecular weights less than 500 Da. However, fornpermeants of molecular weight greater than approximately 500 Da, the size of skin poresnmay be the predominating factor.n" @default.
• W2765865587 created "2017-11-10" @default.
• W2765865587 creator A5037044177 @default.
• W2765865587 date "2017-03-29" @default.
• W2765865587 modified "2023-09-27" @default.
• W2765865587 title "Axoplasmic transport and transepidermal iontophoresis : factors in neurogenic pain management" @default.
• W2765865587 doi "https://doi.org/10.14264/uql.2017.412" @default.
• W2765865587 hasPublicationYear "2017" @default.
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