Search PubMed⌕ Search

Biomedical subjects

T J Maling

Publications and source records attributed to T J Maling.

At least 55 records · Page 3Linked to original sources
PubMed1987

Angiotensin converting enzyme inhibitors and cough.

The relationship between angiotensin converting enzyme inhibitors (ACE inhibitors) and the development of cough was studied in 80 patients. Cough developed in 25 (31%). Seventeen patients had detailed respiratory investigations of whom 12 developed a new cough. Five of the 12 patients had a remission on placebo and recurrence on rechallenge. Cough does occur with ACE inhibitors but there are other possible causes of cough such as asthma, bronchitis, smoking and heart failure. The true incidence of new cough with ACE inhibitors is uncertain at present.

Adult↗
PubMed1987

The relationship between the QT interval and plasma amiodarone concentration in patients on long-term therapy.

We have studied 27 patients on long-term treatment (6-60 months) with amiodarone (dose range 350 mg per week to 2800 mg per week) to ascertain whether the corrected QT interval could predict plasma amiodarone or plasma desethylamiodarone concentration. The patients were assessed on three or four occasions one month apart. There were positive correlations for delta % QTc and plasma amiodarone and delta % QTc and plasma desethylamiodarone. There was approximately a four-fold variation for delta % QTc and plasma amiodarone. This variation was not accounted for by between-occasion variation in the QTc interval, as the coefficient of variation was 2.1%. In six of the patients delta % QTc either decreased or did not change. delta % QTc is not a reliable predictor of plasma amiodarone concentration in the individual patient over time.

Adult↗
PubMed1986

The hemodynamic effects of aminophylline and salbutamol alone and in combination.

We have studied the hemodynamic effects of salbutamol and aminophylline in eight patients with obstructive airways disease. Aminophylline was administered intravenously as a bolus and an infusion for 150 minutes. Salbutamol was administered by nebulizer after 30 minutes and at the end of the infusion. Compared with placebo, salbutamol decreased ventricular afterload (decreased preinjection period and preinjection period to left ventricular ejection time ratio and diastolic blood pressure). Aminophylline decreased total electromechanical systole, corrected for heart rate, only (mean decrease -10.7 msec; range -6.5 to -15.1), indicating a mild positive inotropic effect. When both active treatments were combined, the effect on total electromechanical systole, corrected for heart rate, was potentiated (mean decrease -23.3 msec; range -19.1 to -33.1). Neither aminophylline nor the combination affected heart rate or blood pressure, suggesting no increase in myocardial oxygen consumption. The hemodynamic effects of aminophylline and salbutamol are potentiated in combination but are unlikely to be harmful in patients with obstructive airways disease.

Adult↗
PubMed1985

Distribution of sodium valproate in normal whole blood and in blood from patients with renal or hepatic disease.

Sodium valproate at a concentration of 300 mumol/l in whole blood, partitioned between the red blood cell and plasma to produce a red blood cell/plasma partition ratio of 0.20. Red blood cell uptake was proportional to percent free drug in plasma and uptake was maximal when plasma was replaced by buffer, producing a red blood cell/buffer ratio of 0.87. Reduction of plasma protein binding by plasma dilution, by increasing the total sodium valproate plasma concentration, or by renal or hepatic disease in 24 patients, caused a predictable rise in red blood cell uptake of drug. The red blood cell represented a relatively small compartment for free sodium valproate in blood, however uptake of the drug into this compartment increased considerably in states of reduced plasma protein binding. Because the concentration of drug in the red blood cell reflects free drug concentration in plasma, the red blood cell may serve as an indicator of free drug changes in blood.

Adult↗
PubMed1984

An in-vivo-in-vitro correlation for the bioavailability of frusemide tablets.

The dissolution behaviour of four commercial and two experimental formulations of frusemide tablets has been investigated using the USP rotating basket apparatus and pH 5.0 buffer at 37 degrees C as the test medium. There is a linear relationship between the percentage dissolution in 30 min and the bioavailability relative to an oral solution of frusemide over the bioavailability range 76-97%. Predicted bioavailabilities differed by no more than 2% from the measured values.

Biological Availability↗
PubMed1983

Hypnotic drug prescribing and consumption in a New Zealand teaching hospital.

The relationship between hypnotic drug choice and consumption was investigated with respect to eight variables for eight of the most commonly prescribed hypnotics in Wellington Hospital. The overall prescribing rate was 27% but the dispensing rate was 89.1%, attributable to the high incidence of PRN charting. Consumption of hypnotics increased with increasing patient age and duration of hospital stay. Consumption was higher for medical compared to surgical patients. Drug choice, ward preference and prescribing rate did not influence consumption, highlighting the fundamental discretionary role of the nurse-dispenser, determining the level of consumption.

Adolescent↗
PubMed1980

Sedative and cardiovascular effects of clonidine and nitrazepam.

Five healthy male subjects, aged 26 to 35 yr, received single oral doses of clonidine 0.3 mg, nitrazepam 20 mg, or placebo double-blind with an interval of at least 1 wk between each treatment. Clonodine induced a maximal fall in systo9lic blood pressure from 104.2 +/- 1.6 to 84.7 +/- 1.4 mm Hg (mean +/- SEM) after 3.5 hr and nitrazepam from 102.9 +/- 1.9 to 90.3 +/- 2.6 mm Hg after 1.0 hr while after placebo blood pressure rose steadily from 102.5 +/- 2.9 to 109.6 +/- 3.5 mm Hg at the end of the 8-hr study. Total sleep time increased from 90.3 +/- 2.5. min after placebo to 256.2 +/0 21.0 min after clonidine (p < 0.001) and 281.0 +/- 40.3 min after nitrazepam (p < 0.001). Stage I sleep increased from 49.7 +/- 11.2 to 76.9 +/- 10.2 min after clonidine and to 76.3 +/- 25.2 min after nitrazepam (p < 0.0), while the greatest increase was observed in stage II: 230.7 +/- 25.6 min after clonidine and 236.6 +/- 35.4 min after nitrazepam compared with only 48.5 +/- 15.8 min after placebo (p < 0.001). Plasma norepinephrine did not change after placebo but fell after nitrazepam from 0.28 +/- 0.04 to 0.14 +/- 0.02 ng/ml after 3 hr (p < 0.05) and after clonidine from 0.23 +/- 0.07 to 0.07 +/- 0.02 ng/ml after 2 hr (p < 0.01). Clonidine and nitrazepam both induced similar hypnotic and hypotensive effects with some evidence that this might be due to a reduction in sympathetic tone.

Adult↗