PubMed Health⌕ Search

Biomedical subjects

D N Wade

Publications and source records attributed to D N Wade.

At least 37 records · Page 2Linked to original sources
PubMed1980

Inadvertent intra-arterial injection. A problem of drug abuse.

Peripheral ischaemia related to the inadvertent intra-arterial injection of crushed tablets in suspension, was seen in five drug addicts. Characteristic clinical, features were observed including pain, discolouration, oedema, immediate and delayed sensory and motor deficits, and pregangrenous and gangrenous changes distal to the site of injection. Definitive treatment remains to be established, but an approach to management, based upon probable pathophysiological mechanisms, is proposed.

Adolescent↗
PubMed1980

Cimetidine and acute upper gastrointestinal bleeding: a double-blind controlled trial.

Patients presenting with acute upper gastrointestinal bleeding from a variety of lesions were admitted to a prospective double-blind controlled trial to determine if cimetidine reduces the severity of bleeding and/or the incidence of rebleeding. During the first 48 hours, the patients received intravenous cimetidine (200 mg four-hourly) or placebo, and for the following ten days, oral cimetidine (1 g/24 hr) or placebo. Eight-eight patients entered the trial of whom 45 (51%) were in the cimetidine-treated group. Six of the seven patients requiring surgery for life-threatening bleeding and four of the six patients who rebled were in the cimetidine-treated group. This study failed to demonstrate any advantage of using cimetidine routinely in the treatment of acute upper gastrointestinal bleeding.

Adult↗
PubMed1979

Macrodosage of phenytoin.

Large doses (up to 1200 mg) of phenytoin were required to achieve therapeutic plasma concentrations and to control post-traumatic seizures in a 62-year-old woman. The elimination half-life of phenytoin was calculated to be 3.5 hours. Frequent monitoring of the plasma concentration was essential to optimize the therapeutic control and to avoid systemic toxicity.

Drug Resistance↗
PubMed1979

Chlorbutol toxicity and dependence.

A case of chlorbutol toxicity and dependence is presented. A very long elimination half-life (13.2 days) was found in the patient. The data suggest that chlorbutol is an unsuitable sedative to be available freely to the public.

Adult↗
PubMed1979

Quantitation of plasma warfarin levels by gas chromatography chemical ionization mass spectrometry.

A quantitative assay for plasma concentrations of warfarin has been developed using a deuterated warfarin analogue as internal standard. The method employs methylation (diazomethane) of warfarin to its 4'-methoxy derivative and gas chromatography chemical ionization mass spectrometry. Selected ion monitoring was used to relate the response of warfarin methyl ether and the internal standard. This technique can measure warfarin plasma concentrations five days after a single oral (25 mg) dose. Warfarin half-lives were determined in 12 healthy male volunteers. Each plasma analysis required six minutes of instrument time.

Chromatography, Gas↗
PubMed1979

Plasma quantitation of warfarin and warfarin alcohol by gas chromatography chemical ionization mass spectrometry in patients on warfarin maintenance therapy.

A quantitative method has been developed to measure plasma concentrations of warfarin and warfarin alcohol. The analytical procedure uses deuterated analogues as internal standards, and the technique of selected ion monitoring following gas chromatography methane chemical ionization mass spectrometry of the 4'-methyl ethers of warfarin and warfarin alcohol. Concentrations of warfarin and warfarin alcohol have been measured in plasma samples from 43 patients maintained on chronic warfarin therapy and compared with the 'apparent warfarin' concentration as measured by a fluorometric procedure. The study demonstrated a high degree of correlation between the gas chromatography mass spectrometric derived sum of the individual concentrations of warfarin and warfarin alcohol, and the 'apparent warfarin' concentration determined from a spectrofluorometric assay.

Chromatography, Gas↗
PubMed1979

Phenytoin absorption in patients with ileojejunal bypass.

1 The absorption and elimination of phenytoin was studied after a 200 mg oral dose was administered to seven patients with ileojejunal bypass and nine control patients. 2 Analysis of the area under the plasma concentration time curve showed the absorption of phenytoin was decreased in the subjects with ileojejunal bypass (P less than 0.005). 3 The half life of elimination of the drug was shorter in the bypass group (15.1 h) than in the controls (17.8 h, P less than 0.05). 4 Subjects with an ileojejunal bypass receiving phenytoin are likely to require increased oral dosages to achieve an optimal plasma concentration. There is probably malabsorption of other poorly soluble drugs and parenteral therapy may be necessary to ensure adequate bioavailability.

Adult↗
PubMed1979

Warfarin and warfarin-alcohol levels in anticoagulated patients.

The relationship between dosage, prothrombin ratio, and steady-state plasma concentrations of warfarin and warfarin-alcohol, were determined in 43 patients regularly attending an anticoagulant clinic. The warfarin and warfarin-alcohol concentrations were determined by a gas chromatographic mass spectroscopic (GC/MS) method. A significant correlation was found between the dose and the plasma level of warfarin. There was no significant correlation between the prothrombin ratio and the dose of warfarin, the steady-state plasma levels of warfarin or warfarin-alcohol, or the sum of their plasma concentrations. Measurement of the plasma levels of warfarin and warfarin-alcohol is likely to be of little help clinically other than to detect failure of compliance or malabsorption.

Adult↗
PubMed1979

Comparative study of the dopamine-sensitive adenylate cyclase in the striatum and hypothalamus of rat brain.

Stimulation by dopamine of adenylate cyclase in homogenates of rat brain striatum was enhanced in the presence of ATP (0.6--3 mM) and GTP (10--100 micrometer). The stimulation by dopamine appeared to be the result of its antagonism of inhibition of adenylate cyclase by GTP or higher concentrations of ATP. Stimulation of the enzyme by dopamine was also dependent on MgCl2, and was maximal at MgCl2 concentrations of at least two fold excess over ATP. While ATP did not inhibit adenylate cyclase in homogenates of the ventral hypothalamus, GTP (10--100 micrometer) significantly stimulated it. Dopamine stimulated the adenylate cyclase in the hypothalamus. This action was blocked by chlorpromazine (10 micrometer) and phentolamine (100 micrometer) but not by an analogue of chlorpromazine having no neuroleptic activity or by propranolol (100 micrometer).

Adenosine Triphosphate↗
PubMed1977

Multiple drug interactions with phenytoin.

A 49-year-old female with chronic alcoholism and epilepsy, treated with phenytoin, began to convulse when treatment with disulfiram (an inhibitor of phenytoin metabolism) was discontinued. The patient at this stage was resistant to the large doses of phenytoin, apparently owing to induction of the metabolism of this drug by chronic alcohol intake. Later, a small (30%) increase in dose resulted in about a tenfold increase in plasma concentration of phenytoin and severe toxicity. The final dose of phenytoin required to maintain the plasma level within the therapeutic range suggested that the enzyme induction had decreased. The value of monitoring plasma concentrations of phenytoin is emphasized.

Alcoholism↗
PubMed1977

Mechanisms of inhibition of tolbutamide metabolism: phenylbutazone, oxyphenbutazone, sulfaphenazole.

Tolbutamide half-life was increased by chronic administration of sulfaphenazole (9.5 hr to 28.6 hr, n = 2), phenylbutazone (7.9 hr to 23.1 hr, n = 8), and oxyphenbutazone (8.1 hr to 30.2 hr, n = 2). The rate of elimination of tolbutamide was decreased within 1 to 2 hr of a single dose of sulfaphenazole and the tolbutamide half-life was increased from 9.2 hr to 25.7 hr (n = 2). In contrast, phenylbutazone and oxyphenbutazone, administered as single oral doses of 800 mg, had no immediate effect on tolbutamide elimination. At times greater than 20 to 30 hr after the single dose of phenylbutazone or oxyphenbutazone the rate of tolbutamide elimination was decreased. It is suggested that phenylbutazone and oxyphenbutazone act by inducing form of cytochrome P-450 with low activity for tolbutamide hydroxylation, whereas sulfaphenazole acts by direct inhibition of the microsomal mixed function oxidase system.

Adult↗
PubMed1977

The measurement of histamine release from suspensions of rat peritoneal cells rich in mast cells.

Histamine released from the mast cells in unfractionated rat peritoneal cell suspensions could be quickly and conveniently measured by an automated chemical method. There were no substances in the unfractionated peritoneal cells that interfered with the chemical histamine measurement. Organic extraction of histamine and deproteinization of samples were not necessary using the automated method. The amount of histamine released from preparations of peritoneal cells by a fixed concentration of compound 48/80 decreased with the time of preincubation of the cells but this varied between preparations. Phagocytic activity directed against the mast cells probably explained these observations. The state of nutrition of the rats and the presence or absence and/or glucose in the medium all influenced the rate of decline of viability of the mast cells.

Adenosine Triphosphate↗
PubMed1977

The effect of non-steroidal anti-inflammatory drugs on adenosine triphosphate content and histamine release from rat peritoneal cell suspensions rich in mast cells.

1 Non-steroidal anti-inflammatory drugs (NSAID) suppressed compound 48/80-induced histamine release from rat peritoneal cells in vitro in a dose-dependent manner. 2 NSAID suppressed the adenosine triphosphate (ATP) content of rat peritoneal cells in vitro and this correlated strongly with the suppression of compound 48/80-induced histamine release. 3 The correlation demonstrated suggests that the mechanism of action of NSAID in the rat peritoneal cells is via depletion of cellular ATP.

Adenosine Triphosphate↗