Biomedical subjects

G McKay

Publications and source records attributed to G McKay.

At least 73 records · Page 4Linked to original sources

PubMed1993

The metabolism of piperidine-type phenothiazine antipsychotic agents. III. Mesoridazine in dog, human and rat.

1. The metabolism of mesoridazine was studied in female rats (20 mg/kg, oral), female dogs (50 mg over 30 h, oral) and adult male volunteers (25 mg, oral). 2. Solvent extracts of urines from each species were directly analysed by h.p.l.c.-mass spectrometry with a plasmaspray interface. In the case of phenolic metabolites the urinary extracts were derivatized with a silylating reagent (with and without prior enzymic hydrolysis) prior to analysis. The structures of metabolites, with the exceptions of mesoridazine N-oxide and phenols, were confirmed by comparison of their chromatographic behaviours and mass spectra with those of authentic standards. 3. Compounds identified in the urine of all three species were mesoridazine, sulforidazine, mesoridazine ring sulphoxide, sulforidazine ring sulphoxide, N-desmethylmesoridazine ring sulphoxide, the lactam of sulforidazine ring sulphoxide and phenolic derivatives of mesoridazine and sulforidazine. Whereas the unconjugated phenolic metabolite of sulforidazine was present in urine of all three species, the conjugated form was identified only in dog and rat urines. Also, the unconjugated phenolic metabolite of mesoridazine was identified only in the urine of dog and human, but rat urine contained only the conjugated form. 4. Other metabolites found were: the lactam of mesoridazine (rat), the lactam of mesoridazine ring sulphoxide (rat and human), mesoridazine N-oxide (human) and sulforidazine N-oxide (dog and human). 5. Mesoridazine and six of its metabolites present in urines of human, rat and dog were quantified by a h.p.l.c.-u.v. method. The mean total excretion of measured analytes in human, rat and dog were 6.3, 2.6 and 29.1%, respectively. The excretion of the lactam of sulforidazine ring sulphoxide was greater in human (0.4%) and rat (0.2%) than dog (0.02%). Moreover, the urinary excretion of the lactam of mesoridazine ring sulphoxide in human and rat constituted 0.4% and 0.2%, respectively. Of the three lactams found in rat the lactam of mesoridazine was present in the least amount (0.05%). 6. Interspecies comparison of the lactam metabolites indicated that both qualitatively and quantitatively human more closely resembled rat than dog. On the other hand, N-oxide metabolites were detected in human and dog but not in rat.

Adult↗

PubMed1993

Metabolism of piperidine-type phenothiazine antipsychotic agents. IV. Thioridazine in dog, man and rat.

1. The metabolism of thioridazine was studied in adult male volunteers, female rat and female dog after oral administration of 50 mg, 20 mg/kg and 100 mg over 30 h, respectively. 2. Metabolites in organic extracts of the urine obtained from each species were analysed by plasmaspray h.p.l.c.-mass spectrometry. For phenolic metabolites the crude extracts from each species were derivatized with a silylating reagent (with and without prior enzymic hydrolysis) prior to h.p.l.c.-mass spectrometric analysis. The structures of metabolites, with the exception of phenols, were confirmed by comparison of their chromatographic behaviours and mass spectral data with those of authentic standards. 3. The metabolites identified in the urine of all three species were mesoridazine, sulforidazine, thioridazine ring sulphoxide, mesoridazine ring sulphoxide, sulforidazine ring sulphoxide, the lactam of mesoridazine ring sulphoxide and unconjugated phenolic derivatives of mesoridazine and sulforidazine. Other compounds observed were: unchanged thioridazine (dog, rat), sulforidazine N-oxide (man), N-desmethylthioridazine ring sulphoxide (dog, rat), N-desmethylmesoridazine ring sulphoxide (dog, rat), the lactam of sulforidazine ring sulphoxide (rat, man), phenolic derivative of thioridazine in unconjugated form (rat), and conjugated form (man), and conjugated phenolic derivative of mesoridazine (man). 4. Thioridazine and six of its metabolites present in the urine of man, rat and dog were quantified by a h.p.l.c.-UV procedure. The mean total urinary excretion (+/- SD) of the measured analytes in man, rat and dog were determined to be 4.3 +/- 2.9, 4.8 +/- 1.7 and 12.1 +/- 5.4% of the dose, respectively. The mean excretion of the lactam of mesoridazine ring sulphoxide was greater in man (1.2 +/- 1.0%) and rat (0.2 +/- 0.2%) than dog (< 0.02%). Moreover, the mean excretion of the lactam of sulforidazine ring sulphoxide was quantifiable in both man (0.5 +/- 0.4%) and rat (0.2 +/- 0.2%). 5. Interspecies comparison of the lactam metabolites indicated that both qualitatively and quantitatively, man more closely resembled rat than dog. Similar observations were previously reported for mesoridazine and sulforidazine, therefore rat may be a more suitable animal than dog to undertake further study of the importance of C-oxidation of the piperidine ring of this class of drug.

Adult↗

PubMed1993

Metabolism of phenothiazine and butyrophenone antipsychotic drugs. A review of some recent research findings and clinical implications.

Whereas some metabolites of antipsychotic drugs are psychoactive and contribute to clinical improvement, recent studies have provided evidence that certain metabolites contribute to side-effects which can be disabling enough to negate clinical improvement as regards the psychosis. The route of administration of the drug can determine the amount of metabolite produced in the body and affect how the patient feels in response to the treatment.

Animals↗

PubMed1993

Development of a sensitive and specific radioimmunoassay for benztropine.

A benztropine RIA based on polyclonal antisera raised in New Zealand white rabbits has been developed. The drug-protein conjugates employed had a variety of moles of benztropine hemisuccinate coupled per mole of protein (bovine serum albumin or bovine thyroglobulin). Six antisera were developed and the one with the highest titer was further evaluated for its cross reactivity to N-desmethylbenztropine (4%) and the antipsychotic agents fluphenazine, flupenthixol, chlorpromazine, and haloperidol (all < 1%). The selected antiserum demonstrated sufficient sensitivity to measure benztropine from 0.156 to 100 ng/mL plasma in a 200-microL plasma sample, with a mean CV of < 6%. The RIA was applied to the analysis of steady-state plasma samples obtained from patients undergoing treatment with benztropine and plasma samples obtained from human volunteers and dogs orally dosed with the drug. Both the human and dog plasma samples, when analyzed after hydrolysis with beta-glucuronidase/sulfatase, demonstrated increments in benztropine concentrations, suggesting the drug may be undergoing biotransformation to phase II metabolite(s). In addition, when benztropine was selectively extracted from the unhydrolyzed plasma samples, there was a significant decrease in drug level, which further suggested that the antiserum cross reacted with phase II metabolite(s). The shape of the plasma concentration versus time profile obtained from the dog studies suggested that the drug might also undergo enterohepatic recycling.

Animals↗

PubMed1993

The role of metabolites in a bioequivalence study 1: loxapine, 7-hydroxyloxapine and 8-hydroxyloxapine.

Loxapine is a drug which is used in the treatment of psychotic disorders. The drug is extensively biotransformed in humans to produce a variety of metabolites, some of which have pharmacological activity. Seven-hydroxyloxapine is 4-5 times more active than the parent drug, although its concentrations in plasma are relatively low. Eight-hydroxyloxapine, on the other hand, is inactive, but is present in higher concentrations in plasma than the parent drug. In the present randomized crossover study to evaluate the bioequivalence of two dosage forms containing loxapine, the parent drug and its 7-hydroxy and 8-hydroxy metabolites were monitored for up to 96 hours after the administration of the test or reference formulations. Estimates of average bioavailability (AUC- infinity, AUC0t and Cmax) were obtained by the difference of the least squares means of log test and log reference. A 90% confidence interval for the log difference was derived from the within-subject error. The test of bioequivalence requires the 90% confidence band so calculated to fall entirely within an imposed regulatory interval of 80-125%. The results showed the two formulations to be bioequivalent in terms of the log mean differences and 90% confidence bands calculated for all three analytes. In fact, the within-subject variabilities of the metabolites were relatively low, so that the 90% confidence intervals for ln AUC0 infinity, ln AUC0t and ln Cmax calculated for the metabolites, were narrower that those for the parent drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1992

Synthesis and characterization of quaternary ammonium-linked glucuronide metabolites of drugs with an aliphatic tertiary amine group.

A synthetic approach was developed to make the quaternary ammonium-linked glucuronide metabolites of compounds with an aliphatic tertiary amine group. The key step involved quaternization of the compound with methyl (2,3,4-tri-O-acetyl-alpha-D-glucopyranosyl bromide)uronate and sodium bicarbonate in a two-phase system of water and an organic solvent. The synthetic approach successfully yielded quaternary ammonium-linked glucuronides of 20 drugs and two of their phase I metabolites. The drugs were from various pharmacological classes: H1 antihistamines, antipsychotic agents, and tricyclic antidepressants. Physical data such as HPLC retention times, and diagnostic fast-atom bombardment mass spectra and 1H NMR spectra were obtained. These should aid in the characterization of compounds in samples isolated from biological media.

Amines↗

PubMed1992

Stereoselective pharmacokinetics of doxepin isomers.

Commercial preparations of the tricyclic anti-depressant doxepin contain 15% of the more active cis-doxepin and 85% of the trans-isomer. The single dose pharmacokinetics of doxepin and its major metabolite N-desmethyldoxepin were examined in 30 healthy young men. Results for total doxepin showed wide intersubject variation in all pharmacokinetic parameters except tmax and Cmax. Plasma levels of cis-doxepin were extremely low and it was only possible to estimate the stereoselective pharmacokinetics of the parent drug in 3 subjects. The data from those particular subjects resulted in an average ratio of cis- to trans-doxepin isomers in plasma of 15:85. In contrast, the mean plasma levels of cis-N-desmethyldoxepin in 28 subjects exceeded those of the trans-isomer at every time point after 10 h, such that the areas under the plasma concentration versus time curves (AUC) of cis-N-desmethyldoxepin were significantly higher than those of the corresponding trans-isomer. This phenomenon may play an important role in the therapeutic action of doxepin since it has been suggested that cis-N-desmethyldoxepin is pharmacologically active. In 2 subjects, however, the AUC0-inf of trans-N-desmethyldoxepin were respectively 4 and 8 fold higher than those of the cis-isomer.

Adolescent↗

PubMed1992

The metabolism of piperidine-type phenothiazine antipsychotic agents. I. Sulforidazine in the rat.

1. The metabolism of the piperidine-type, phenothiazine antipsychotic agent, sulforidazine, was studied in female rats after a 20 mg/kg single oral dose. 2. Compounds identified in urine were sulforidazine, sulforidazine ring sulphoxide, the lactam of sulforidazine, the lactam of sulforidazine ring sulphoxide, two diastereomers of N-desmethylsulforidazine ring sulphoxide and a phenolic derivative of sulforidazine. 3. Metabolites were separated by h.p.l.c. prior to mass spectrometric or g.l.c.-mass spectrometric analysis. Except in the case of the phenolic metabolite, structures were confirmed by direct comparison of electron impact mass spectra and chromatographic behaviour with those of authentic samples. To facilitate identification of the phenolic metabolite the crude urinary extract was treated with a silylating reagent and analysed by h.p.l.c.-mass spectrometry with a plasmaspray interface. 4. Despite the availability of authentic standards of sulforidazine N-oxide and sulforidazine N,S-dioxide neither of these compounds could be identified in urinary extracts obtained from rats. 5. Sulforidazine underwent extensive metabolism in rats as only 2.3 +/- 0.4% (n = 5) of the dose was present as unchanged sulforidazine in 24 h urine. The lactam of sulforidazine (0.1 +/- 0.1%) was a minor metabolite whereas the lactam of sulforidazine ring sulphoxide was 3.2 +/- 2.6% dose. 6. Sulforidazine sulphoxide (12.1 +/- 1.6%) was a major metabolite and its diastereomers were present in similar amounts.

Animals↗

PubMed1991

In vitro hydrolysis of RR,SS-threo-methylphenidate by blood esterases--differential and enantioselective interspecies variability.

Enantioselective in vitro hydrolysis of methylphenidate (MPH) by the blood esterases of seven mammalian species is reported. The species included rats, rabbits, dogs, cattle, horses, monkeys, and humans. In vitro incubations up to 8 h were carried out in plasma, red blood cells, and whole blood of the various species. Enantioselective differences were evident among the different species on comparison of the data obtained from the three biological fluids. The esterases present in plasma appeared to show greater activity in the hydrolysis of MPH in all species where comparison with the other two biofluids was possible. Only in the case of humans did esterases present in plasma and red blood cells demonstrate opposite enantioselectivity in the hydrolysis of MPH. Thus after 8 h incubation, the RR-MPH/SS-MPH ratios in plasma and red blood cells were 0.31 and 1.16, respectively.

Animals↗

PubMed1991

Quinidine but not quinine inhibits in man the oxidative metabolic routes of methoxyphenamine which involve debrisoquine 4-hydroxylase.

Healthy male volunteers (n = 13) took a single oral dose of 60.3 mg of methoxyphenamine HCl with and without prior administration of either quinidine (250 mg as bisulphate salt) or its diastereomer quinine (300 mg as sulphate salt). Methoxyphenamine and its N-desmethyl, O-desmethyl and aromatic 5-hydroxy metabolites were quantified in the 0-32 h urine. The oxidative routes of methoxyphenamine metabolisms which had been previously shown to involve debrisoquine 4-hydroxylase, namely O-demethylation and 5-hydroxylation were both significantly inhibited by quinidine in the 12 extensive metabolizers. The inhibition was selective in that N-demethylation which does not involve this isozyme was not affected by quinidine. In all but one of these volunteers the methoxyphenamine/O-desmethylmethoxyphenamine ratio changed such that extensive metabolizers could be classified as poor metabolizers due to quinidine pretreatment. No marked change occurred in the renal excretion of methoxyphenamine and its three metabolites either in the extensive metabolizers because of quinine pretreatment or in the poor metabolizer because of treatment with either quinidine or quinine. Thus in the extensive metabolizer phenotype it was demonstrated in one study that enzyme inhibition of quinidine was selective in terms of the metabolic pathways inhibited as well as stereoselective with respect to the inhibitor.

Adult↗

PubMed1991

Pharmacodynamic effects of buspirone and clobazam.

1. The pharmacodynamic effects of buspirone and clobazam were compared in two volunteer studies. Acute doses of buspirone 5 mg, 10 mg and clobazam 10 mg were contrasted with placebo and a verum (lorazepam 1 mg), in a repeated measures design with 10 subjects assessed on a battery of psychometric tests at 1.5, 3.5, and 5.5 h post dose. For the combined results clobazam and the lower dose of buspirone (5 mg) were significantly contrasted with lorazepam on measures of subjective sedation, memory and choice reaction time (CRT). The higher dose of buspirone was not statistically different from lorazepam for all measures except memory; whilst contrasting significantly with placebo and clobazam on movement and total reaction time components respectively. Though failing to achieve significance, a similar trend was seen for critical flicker fusion (CFF) with buspirone 10 mg and lorazepam producing the lowest scores indicative of increased sedation. 2. Repeated doses of buspirone 5 mg twice daily, clobazam 10 mg twice daily, or placebo twice daily for 8 consecutive days were compared on the same battery of psychometric tests in a repeated measures design. Nine subjects were assessed on days 1, 3, and 8 of the study. Overall, memory performance significantly decreased with buspirone 5 mg in contrast to both clobazam and placebo whilst the opposite trend was seen with CFF. Clobazam significantly improved TRT in contrast to both placebo and buspirone. 3. These results indicate improved reaction time and memory performance with repeated dosing of clobazam in contrast to buspirone. Impairment following acute administration of buspirone appears limited to the higher (10 mg) dose.

Adult↗

PubMed1991

Plasma levels of fluphenazine in patients receiving fluphenazine decanoate. Relationship to clinical response.

The levels of fluphenazine and fluphenazine sulphoxide in schizophrenic patients who were randomly assigned to receive either 5 mg or 25 mg of fluphenazine decanoate every two weeks were monitored. Patients treated with 25 mg of fluphenazine decanoate required three months to reach a steady-state plasma level, indicating that those patients who are being converted from oral to depot fluphenazine should continue to receive oral supplementation during the first three months of treatment with fluphenazine decanoate. Plasma levels of fluphenazine sulphoxide were lower than levels of fluphenazine. At six and nine months following randomisation, there was a statistically significant relationship between lower fluphenazine plasma levels and an increased risk of psychotic exacerbations. A relatively weak relationship was found between fluphenazine plasma levels and akinesia, but non-significant relationships between fluphenazine levels and other neurological side-effects including akathisia, retardation, and tardive dyskinesia. Monitoring the plasma levels may be helpful to clinicians who are attempting to treat stabilised patients with the lowest effective dose of fluphenazine decanoate.

Adult↗

PubMed1991

N(+)-glucuronidation of aliphatic tertiary amines, a general phenomenon in the metabolism of H1-antihistamines in humans.

1. Representative drugs of the various structural classes of H1 antihistamines were chosen for study. The drugs chosen (class name in parentheses) were chlorpheniramine maleate and pheniramine maleate (alkylamines), diphenhydramine hydrochloride and doxylamine succinate (ethanolamines), pyrilamine maleate and tripelennamine hydrochloride (ethylenediamines), promethazine hydrochloride (phenothiazine), cyclizine lactate (piperazine) and terfenadine (miscellaneous). In each case oral dose(s) were administered over no more than 6 h to two healthy volunteers and the total urine collected for 36 h. 2. Metabolites from urine were separated by h.p.l.c. and individually collected prior to mass spectrometric analysis in the fast atom bombardment mode. The structure of each metabolite identified as a quaternary ammonium-linked glucuronide metabolite was confirmed by direct comparison of its mass spectrum and chromatographic behaviour with that of a synthetic authentic compound. 3. For eight of the nine drugs studied, metabolism by the N(+)-glucuronidation pathway was observed in each of the volunteers. Terfenadine was the exception. 4. The amount of each N(+)-glucuronide in the urine was estimated by h.p.l.c. analysis. The mean proportion of dose excreted as the metabolite was 14.3%, 6.5% and 4.0% for cyclizine, tripelennamine and diphenhydramine, respectively. Promethazine was the only case where the N(+)-glucuronide accounted for less than 1.0% of the administered dose in both volunteers examined.

Adult↗

PubMed1991

Quinine is a more potent inhibitor than quinidine in rat of the oxidative metabolic routes of methoxyphenamine which involve debrisoquine 4-hydroxylase.

1. Lewis rats (n = 7 or 8) were dosed with methoxyphenamine with and without prior administration of various doses of either quinine or its diastereomer quinidine. Methoxyphenamine and its N-desmethyl, O-desmethyl and aromatic 5-hydroxy metabolites were quantified in 0-24 h urine. 2. The oxidative routes of methoxyphenamine metabolism which had been previously shown to involve the debrisoquine/sparteine isoenzyme, namely O-demethylation and 5-hydroxylation, were both significantly inhibited by quinine. The inhibition was selective in that N-demethylation which does not involve this isoenzyme was not affected by quinine. 3. Quinidine which had been previously shown at a relatively high dose (80 mg/kg) to affect the three metabolic routes of methoxyphenamine in a similar fashion was ineffective in this regard at a 25 mg/kg dose. Quinine more effectively inhibited the O-demethylation and 5-hydroxylation of methoxyphenamine than did quinidine, and its inhibition was marked at the lowest dose examined, 12.5 mg/kg. 4. As quinidine is a more potent inhibitor than quinine of debrisoquine 4-hydroxylase in man, the rat should be used only with full realization of its limitations when investigating substrates metabolized by this isoenzyme.

Animals↗

PubMed1991

The metabolites of chlorpromazine N-oxide in rat bile.

1. The metabolism of chlorpromazine N-oxide was studied in female rats after a 20 mg/kg single i.p. dose. 2. Metabolites identified in urine and faeces were chlorpromazine, 7-hydroxychlorpromazine, chlorpromazine sulphoxide, N-desmethylchlorpromazine and N-desmethylchlorpromazine sulphoxide. As these same five metabolites were previously shown to be present after oral administration this indicates that reduction of chlorpromazine N-oxide occurs not only in the gastrointestinal tract but also at other sites. 3. The metabolism of chlorpromazine N-oxide was studied following its administration by either i.p., i.v. or oral routes to female rats in which the bile duct was cannulated. 4. There were no qualitative differences between the three routes of administration with respect to the metabolites identified. With the exception of the absence of N-desmethylchlorpromazine and N-desmethylchlorpromazine sulphoxide, all metabolites previously identified in urine and faeces were also present in bile. 5. Additionally there were three compounds present in rat bile which were not identified in urine or faeces. These were chlorpromazine N-oxide, chlorpromazine N,S-dioxide and 7-hydroxychlorpromazine O-glucuronide. This is the first unequivocal evidence for the identification of intact 7-hydroxychlorpromazine O-glucuronide in any species. 6. The inability to detect chlorpromazine N-oxide and chlorpromazine N,S-dioxide in the faeces of rats is likely to be due to the reduction of the N-oxide group on the passage of these biliary metabolites down the intestinal tract.

Animals↗

PubMed1990

Comparative bioavailability of two tablet formulations of fluphenazine dihydrochloride in drug-free psychiatric patients.

The comparative bioavailability of a new tablet formulation of fluphenazine dihydrochloride (5 mg) and a reference product (fluphenazine dihydrochloride, Prolixin, 5 mg) was assessed in drug-free psychiatric patients. Twenty-six patients were initially entered in the study, of whom 22 completed the protocol. Each patient received the test (T) and the reference formulation (R) in a balanced two-way crossover design. Plasma concentrations of fluphenazine were monitored over a period of 48 h after drug administration using a sensitive HPLC method. One patient did not show any measurable plasma concentration for one formulation at any sampling time and, therefore, bioavailability was assessed in the remaining 21 patients. All pharmacokinetic parameters showed wide intersubject variation. The maximum plasma concentration (Cmax), time to Cmax, and area under the curve up to the last measurable concentration (AUClast0), infinity (AUCinfinity0), or truncated areas (such as AUC16(0), AUC24(0) were compared by analyses of variance and found not to be significantly different in each case across the formulations. Except for AUC24(0), AUC32(0), and AUC48(0), ANOVA of all other parameters showed a high power (greater than 80%) to detect a 20% difference in the mean value of each bioequivalence parameter between T and R. The two formulations were found to be bioequivalent in that confidence intervals of the mean values of AUCinfinity0, AUClast0, truncated AUCs, or Cmax for T:R ratios were, in each case, well within the acceptable range of 100 +/- 20%.

Biological Availability↗

PubMed1990

Bioequivalence of two thorazine tablet formulations using radioimmunoassay and gas chromatographic-mass spectrometric methods.

Two analytical methods for the analysis of chlorpromazine (CPZ), a radioimmunoassay (RIA) and a GLC-MS method, were compared in a bioequivalence study of two CPZ tablet formulations (Thorazine: film coated and sugar coated). Thirty-six nonsmoking, healthy, male volunteers completed the study. Each subject ingested single doses (2 x 25 mg) of the test (T) and the reference (R) formulations in a two-way crossover design with a two-week drug-free interval between doses. Following each administration, plasma concentrations of CPZ were monitored over a period of 24 h by both RIA and GLC-MS methods. Plasma concentrations and pharmacokinetic parameters determined by either analytical method showed wide intersubject variation, with the GLC-MS data showing relatively higher magnitude of intersubject variation than the RIA data. In general, plasma concentrations measured by RIA were significantly different from those measured by GLC-MS (paired t tests: p less than 0.0001). As indicated by the regression analysis, concentrations determined by RIA were 1.3-1.4 times higher than those determined by GLC-MS. There were strong and significant correlations between the two methods for both T and R (r greater than 0.75: p less than 0.0001). Similar statistical relationships were found between the plasma concentrations of CPZ determined by the two methods at each sampling time and the bioequivalence parameters area under the plasma level versus time curves up to the last measurable concentration (AUCt0) and the maximum plasma concentration (Cmax).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Development and application of a radioimmunoassay for fluphenazine based on monoclonal antibodies and its comparison with alternate assay methods.

The development of a monoclonal antibody towards fluphenazine allows the measurement of plasma concentrations of this highly potent neuroleptic. The method demonstrates sufficient sensitivity to measure 0.02 ng of fluphenazine per milliliter of plasma and employs a 150-microL plasma extract derived from a 2-mL plasma sample. The procedure is linear over the concentration range of 0.02 to 2.5 ng/mL, with a mean overall coefficient of variation of less than 3%. The validity of the described monoclonal-based RIA procedure was confirmed by comparison to alternate assay methods in replicate samples. Comparison to a newly developed HPLC-coulometric procedure in 159 samples showed a strong correlation, with a slope value of close to unity (1.0484) and a coefficient of correlation of 0.8136, while comparison to a previously developed polyclonal-based RIA procedure showed a correlation of 0.95 and a slope of 0.91 (n = 26).

Animals↗