Determination of barbiturates by automatic differential spectrophotometry

Williams, Louis A.; Zak, B A Lydia

doi:10.1016/0009-8981(59)90126-3

Cited by 39 publications

(6 citation statements)

References 7 publications

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“…Figure 2 the results of such studies are presented for two membranes. The relation between the apparent A and the degree of dissociation is linear (Williams & Zak, 1959). These experiments gave identical results with our usual method, yielding for phosphatidylcholine vesicles a AA-of 9 + 2.5.…”

Section: Methodssupporting

confidence: 79%

“…The magnitude of the partition coefficient for the anion was not entirely expected and was accordingly checked in experiments with multilamellar vesicles, which were separated from buffer after equilibration by either centrifugation or ultrafiltration. In addition to scintillation counting a spectroscopic assay of the barbiturate was also employed (Williams & Zak, 1959). These experiments gave identical results with our usual method, yielding for phosphatidylcholine vesicles a AA-of 9 + 2.5.…”

Section: Resultsmentioning

confidence: 62%

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THE DEPENDENCE OF THE LIPID BILAYER MEMBRANE: BUFFER PARTITION COEFFICIENT OF PENTOBARBITONE ON pH AND LIPID COMPOSITION

Miller

1977

British J Pharmacology

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The membrane/buffer partition coefficient of [14C]‐pentobarbitone has been determined as a function of the lipid composition of bilayer membranes. A new technique based on ultrafiltration gave comparable results to conventional techniques but required less time for equilibration. The membrane/buffer coefficient was independent of pentobarbitone concentration in the range studied. The apparent partition coefficient varied with pH and was a linear function of the degree of dissociation of pentobarbitone. Both the charged and uncharged forms of pentobarbitone partitioned into the membrane, the latter to a much greater extent than the former. At low pH the highest partition coefficient observed was in egg phosphatidylcholine bilayer membranes. Incorporation of cholesterol or phosphatidic acid into phosphatidylcholine membranes greatly reduced the partition coefficient. High pressures do not greatly change these partition coefficients.

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Section: Methodssupporting

confidence: 79%

Section: Resultsmentioning

confidence: 62%

THE DEPENDENCE OF THE LIPID BILAYER MEMBRANE: BUFFER PARTITION COEFFICIENT OF PENTOBARBITONE ON pH AND LIPID COMPOSITION

Miller

1977

British J Pharmacology

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“…For more than a decade, barbiturate concentrations in biological fluids and tissues have been determined in this laboratory initially by the Goldbaum's method ( 1) and later by the modified DV differential method (2). Qualitatively, crystal tests and paper chromatography (3) have been replaced by gas(4),(5),(6) and thin layer chromatography(7), (8).…”

Section: Resumementioning

confidence: 99%

Comparison of the UV Differential and the GLC Methods for the Quantitation of Barbiturates in Blood

Yen¹,

Cimbura²

1976

Canadian Society of Forensic Science Journal

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“…Awakening brain levels of barbiturate in challenged animals were determined as an index of central nervous system sensitivity to the drugs, by means of a spectrophotometric method (Stolman & Aston, 1970) based upon the technique of Williams & Zak (1959). In addition, hepatic pentobarbitone-metabolizing activity was determined in unchallenged rats from each of the 12 pretreated groups, by the method of Kato & Chiesara (1962), to determine possible changes in the metabolic disposition of barbiturates.…”

Section: Methodsmentioning

confidence: 99%

Mechanisms contributing to barbiturate intolerance in rats

Aston¹

1973

British J Pharmacology

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Summary Female rats, 3 weeks after pretreatment with 200 or 400 (mg/kg)/day barbitone for 2 or 30 days, exhibited a prolonged sleeping time and a reduced awakening barbiturate brain level when challenged with either barbitone or pentobarbitone. After 3 additional weeks, the latter responses had returned, or were returning to, control values. Barbitone pretreatment schedules had no residual effect upon in vitro hepatic pentobarbitone‐metabolizing activity measured 3 or 6 weeks later, except in one instance, when hepatic enzyme activity was significantly enhanced 3 weeks after 30 daily doses of 200 mg/kg barbitone. In this case, however, an enhanced barbiturate sleeping time, together with a reduced awakening barbiturate brain level, were observed. It is concluded that barbitone administered intraperitoneally in doses of 200 to 400 (mg/kg)/day for 2 or 30 days induces a non‐hepatogenic intolerance to barbiturates, related to an increased sensitivity of the central nervous system to these drugs. This central intolerance is seen 3 weeks, but not 6 weeks, after pretreatment. Furthermore, this central intolerance has been observed to co‐exist with an hepatic tolerance, a situation which could result in a reduced LD50 coupled with an increase in ED50.

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Determination of barbiturates by automatic differential spectrophotometry

Cited by 39 publications

References 7 publications

THE DEPENDENCE OF THE LIPID BILAYER MEMBRANE: BUFFER PARTITION COEFFICIENT OF PENTOBARBITONE ON pH AND LIPID COMPOSITION

THE DEPENDENCE OF THE LIPID BILAYER MEMBRANE: BUFFER PARTITION COEFFICIENT OF PENTOBARBITONE ON pH AND LIPID COMPOSITION

Comparison of the UV Differential and the GLC Methods for the Quantitation of Barbiturates in Blood

Mechanisms contributing to barbiturate intolerance in rats

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