By Ciba Foundation Symposium 26
Chapter 1 Chairman's advent (pages 1–3): Alan S. Curry
Chapter 2 The Clinician's necessities from the Laboratory within the therapy of the Acutely Poisoned sufferer (pages 5–15): R. W. Newton
Chapter three The function of the Laboratory within the remedy of Narcotic Poisoning (pages 17–28): Vincent P. Dole
Chapter four Formation of Reactive Metabolites as a reason for Drug Toxicity (pages 29–55): James R. Gillette
Chapter five Separation and Detection of risky Metabolites of Amphetamines, Analgesics and Phenothiazines (pages 57–82): A. H. Beckett
Chapter 6 review of Chromatographic and Spectroscopic systems (pages 83–103): A. C. Moffat
Chapter 7 Use of fuel Chromatography?Mass Spectrometry in Toxicological research (pages 105–124): Bo Holmstedt and Jan?Erik Lindgren
Chapter eight choice of hashish elements in Blood (pages 125–137): Stig Agurell
Chapter nine Drug Assay via Radioactive Reagents (pages 139–154): W. Riess
Chapter 10 An On?Line Liquid Chromatograph?Mass Spectrometer approach (pages 155–169): R. P. W. Scott, C. G. Scott, M. Munroe and J. Hess
Chapter eleven Luminescence tools in Drug research (pages 171–192): J. W. Bridges
Chapter 12 Immunoassay of gear (pages 193–200): Irving Sunshine
Chapter thirteen Immunological tools for Detecting medicines: their software within the Detection of Digitoxin, Digoxin and Morphine (pages 201–217): Charles W. Parker
Chapter 14 Drug research within the Overdosed sufferer (pages 219–238): B. Widdop
Chapter 15 The Morbid Anatomist's position in Drug Detection (pages 239–251): D. J. Gee
Chapter sixteen Drug?Induced Iatrogenic ailment: the chance of its Detection (pages 253–268): Henry Leach
Chapter 17 boundaries of Haemodialysis and compelled Diuresis (pages 269–289): L. F. Prescott
Chapter 18 The Poisoned sufferer: The Clinician and the Laboratory (pages 291–314): Roy Goulding
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Extra info for Ciba Foundation Symposium 26 - The Poisoned Patient: The Role of the Laboratory
By contrast, when the reactive metabolite is sufficiently stable to leave the organ in which it is formed, the rate of covalent binding of the reactive metabolite will depend on many interrelated factors: (1) the chemical reactivity of the metabolite, (2) the diffusibility of the metabolite, (3) the rate of blood flow to the various tissues, and (4) the activities of the enzymes that catalyse the formation and inactivation of the reactive metabolites in the various tissues. Obviously, pharmacokinetic equations that included these interrelationships 38 JAMES R.
Some of the effects, however, may seem unusual to those familiar only with the pharmacokinetics of reversibly acting drugs. To learn what might be expected after a given treatment, it is perhaps useful to review the basic principles of the kinetics of covalent binding of reactive metabolites to macromolecules in the body (Gillette 1973). The pharmacokinetic equations shown in Fig. 1 were derived on I IV k13 ko ‘T eo (2) (%) = Att= IV, 03 = Qo LetAIV, k34 111 , IV (1 - Ee-at + Fe-ct) k34 k34 (%) (2) k13 a - k13 kio + .
In this situation, any treatment that specifically altered the activity of the enzyme catalysing the formation of the major metabolite in the tissue that metabolized most of the drug in the body would alter the denominator of the A ratios in all the other tissues, even if that treatment did not affect enzyme activities in the other tissues. For example, when the major pathway of elimination of a foreign compound is through the formation of its reactive metabolite in the liver, a substance that induces only the liver enzyme may tend to increase the covalent binding of the reactive metabolite in the liver and decrease it in other tissues, whereas a substance that inhibits the enzyme only in the liver would tend to decrease the covalent binding in the liver but increase it in the other tissues.