Construction and performance characteristics of new ion selective electrodes based on carbon nanotubes for determination of meclofenoxate hydrochloride.

This work offers construction and comparative evaluation the performance characteristics of conventional polymer (I), carbon paste (II) and carbon nanotubes chemically modified carbon paste ion selective electrodes (III) for meclofenoxate hydrochloride are described. These electrodes depend mainly on the incorporation of the ion pair of meclofenoxate hydrochloride with phosphomolybdic acid (PMA) or phosphotungestic acid (PTA). They showed near Nernestian responses over usable concentration range 1.0 × 10(-5) to 1.0 × 10(-2)M with slopes in the range 55.15-59.74 mV(concentrationdecade)(-1). These developed electrodes were fully characterized in terms of their composition, response time, working concentration range, life span, usable pH and temperature range. The electrodes showed a very good selectivity for Meclo with respect to a large number of inorganic cations, sugars and in the presence of the degradation product of the drug (p-chloro phenoxy acetic acid). The standard additions method was applied to the determination of MecloCl in pure solution, pharmaceutical preparations and biological samples. Dissolution testing was also applied using the proposed sensors.

A simple and sensitive HPLC method for quantification of the metabolin of meclofenoxate in human plasma.

A simple and sensitive high-performance liquid chromatographic method was developed for quantification of the metabolin of meclofenoxate, chlorophenoxyacetic acid, in human plasma. Ibuprofen was used as an internal standard. The present method used protein precipitation for extraction of chlorophenoxyacetic acid from human plasma. Separation was carried out on a reversed-phase C(18) column. The column effluent was monitored by UV detection at 254 nm. The mobile phase was a mixture of methanol and water containing 1.0% glacial acetic acid (70:30 v/v) at a flow rate of 1.0 mL/min. The column temperature was 20 degrees C. This method was linear over the range of 0.047-28.20 microg/mL with a regression coefficient greater than 0.99. The mean recovery of chlorophenoxyacetic acid and IS were (79.54 +/- 6.33)% and (78.48 +/- 2.14)%, respectively, and the method was found to be precise, accurate, and specific during the study. The method was successfully applied for pharmacokinetic study of chlorophenoxyacetic acid in human.

Kinetics of hydrolysis of meclofenoxate hydrochloride in human plasma.

The kinetics of hydrolysis of meclofenoxate hydrochloride in human plasma have been compared with those of clofibrate. The hydrolysis rate in fractionated plasma was determined in the presence and absence of a plasma esterase inhibitor, tetraethyl pyrophosphate. The kinetic data indicated that clofibrate decomposed only by esterase-induced hydrolysis, which was inhibited by binding of clofibrate to plasma proteins. In contrast to clofibrate, meclofenoxate decomposed rapidly in human plasma via spontaneous hydrolysis as well as esterase-induced hydrolysis. The spontaneous hydrolysis appeared to be inhibited by some components present in the esterase fraction isolated from plasma, while no significant inhibition of the hydrolysis by protein binding was observed.

Effects of various cerebral metabolic activators on glucose metabolism of brain.

The effects of various metabolic activators on the glucose metabolism of the perfused cat brain have been investigated. (1) When the perfusion is done with the blood containing cytidine monophosphate, the glucose metabolism of the brain is enhanced, as compared to the perfusion with the blood without cytidine monophosphate. There is no marked change in the cerebral metabolic rate and in the contents of intermediate metabolite of glucose in the brain. (2) Citicoline enhances the incorporation of blood glucose into the brain and its metabolism in the brain. It increases slightly the cerebral blood flow rate and decreases the accumulation of lactate in the brain. (3) Either Pyrithioxin or Meclophenoxate has no effect on the glucose metabolism of the brain nor on the cerebral metabolic rate.