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Biomedical subjects

M T Vicente

Publications and source records attributed to M T Vicente.

7 recordsLinked to original sources

A computer program (DCN) for numerical convolution and deconvolution of pharmacokinetic functions.

A program adapted for use on microcomputers (DCN) has been developed which permits one to perform operations of numerical convolution and deconvolution using polyexponential functions, that are often implemented in pharmacokinetic analysis. The program is written in Microsoft GWBASIC and can be used in personal computers with no modification. The user supplies information relating to the coefficients and exponentials defining the polyexponential equation of the response and weighting functions and the program performs the deconvolution operation by numerical integration using trapezoidal rule and provides numerical and graphic information concerning the input function. The program can be applied to the deconvolution of many linear pharmacokinetic systems and allows one to solve problems related to drug release, absorption, distribution, as well as others. Additionally, the program is able to perform the convolution operation if information about the input and weighting functions and is also able to simulate pharmacokinetic processes. The efficacy of the program was evaluated by comparison with several deconvolution algorithms, in particular that proposed by Veng-Pedersen and Iga.

Algorithms↗

Serum lidocaine levels in patients undergoing fibrobronchoscopy.

Serum lidocaine levels were determined in 29 patients undergoing fibrobronchoscopy after drug doses ranging from 180 to 400 mg. The results showed rapid absorption of the anaesthetic by the tracheobronchial mucosa with an average absorption constant of 4.77 +/- 1.99 h-1. Maximum lidocaine levels in serum averaged 1.21 +/- 0.64 microgram/ml, lower than the levels established as toxic for this anaesthetic. The serum half-life of lidocaine averaged 1.55 +/- 0.72 h. The percentage of dose absorbed in this kind of patient ranged between 20.89 and 60.88% of the dose administered.

Absorption↗

IR and X-ray diffraction study of chlorpheniramine maleate-montmorillonite interaction.

As a contribution to studies on the adsorption of drugs by clay minerals aimed at achieving sustained action in the oral administration of antihistamines, the adsorption of chlorpheniramine maleate by sodium montmorillonite was studied by X-ray diffraction and IR spectroscopy. The results indicated that the chlorphenirammonium ion penetrated into the interlayer space of montmorillonite, producing an increase in the basal spacing, d001, of the silicate. This increase was influenced, as was the amount adsorbed, by the pH and the concentration of the chlorpheniramine maleate solution. At pH 7.0, the amount adsorbed was close to the exchange capacity, and the complex formed had a basal spacing of 17.14 A (delta = 7.54 A). The only mechanism responsible for the interaction was cation exchange. The complex at 17.14 A must be a monolayer with the benzene rings positioned perpendicular to the surface of the oxygen atoms.

Bentonite↗

Pharmacokinetics of cefazolin administered as a new drug delivery system in healthy volunteers.

A study was made of the pharmacokinetic behaviour in plasma and urine of cefazolin in seven healthy volunteers following parenteral administration of sodium cefazolin (1250 mg) and a sustained release formulation containing sodium cefazolin: cefazolin-dibenzylamine (1:4) at a total dose of 1250 mg, both formulations being administered over 1 week by the i.m. route. Cefazolin concentrations in plasma and urine were determined by a HPLC technique. Kinetic analysis of the experimental results was performed using an open single-compartment kinetic model and a sustained release model for the drug administered as standard formulation and the sustained release formulation, respectively. The results obtained point to significant variations in the pharmacokinetic profile of the drug when administered in the DDS. The time of cefazolin at levels greater than 1 microgram ml-1 was 16.03 +/- 2.51 and 47.76 +/- 14.18 h-1 after administration of the standard formulation and the DDS, respectively. The urinary excretion rate curves also show the existence of sustained drug levels in the urine following administration of the DDS. The renal clearance of the drug did not show statistically significant differences between the two formulations administered. The process of release of cefazolin from the cefazolin-dibenzylamine complex proved to be a first order kinetic process. The release constant of the antibiotic was calculated according to three different methods: the Wagner-Nelson method; the statistical moments method; and the fitting of the plasma levels curves to a compartmental model considering release and absorption. The values obtained for this constant ranges from 0.026 +/- 0.02 h-1 calculated with the method of statistical moments to 0.094 +/- 0.03 h-1 as calculated by the equation derived for the plasma fitting of cefazolin administered as DDS.

Adult↗

Catecholamine and MHPG plasma levels, platelet MAO activity, and 3H-imipramine binding in heroin and cocaine addicts.

This work evaluated in a population of heroin and heroin plus cocaine human addicts: 1. Norepinephrine (NE), epinephrine (Epi) and 3-methoxy-4-hydroxyphenylglycol (MHPG) (the principal metabolite of brain NE) plasma levels; 2. Monoamine oxidase (MAO) activity; and 3. 3H-imipramine specific binding to the amine carrier in platelets. NE plasma levels were significantly lower in the short-term heroin user groups (1-3 and 4-6 yr), a finding not observed in both long-term heroin user ( > 6 yr) and heroin plus cocaine user ( > 6 yr) groups. Epi levels changed in a similar manner, except that a significant increase was noted in heroin plus cocaine abusers. Conversely, dopamine and MHPG plasma levels increased with the duration of heroin use, and even more with cocaine abuse. Platelet MAO activity increased in all groups. Specific 3H-imipramine binding sites showed an increase after 3 yr of heroin abuse and in all heroin plus cocaine addicts. In conclusion, short-term use of heroin decreases NE or Epi release, but with prolonged use, a slow adaptation occurs. In contrast, cocaine inhibits the neuronal Epi uptake, even in a situation of long duration of abuse. Probably the amine levels additionally regulate the amine carrier, resulting in changes that show a different pattern from major depression. These drugs of abuse may also influence directly or indirectly related enzymatic systems.

Adult↗