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Biomedical subjects

K Weerasuriya

Publications and source records attributed to K Weerasuriya.

10 recordsLinked to original sources
PubMed1990

'Codes' and practice: information in drug advertisements--an example from Sri Lanka.

The amount of scientific information that should appear in an advertisement for a drug has been discussed for over 20 years. The information should promote the rational use of the drug. There is a lack of data from developing countries. We analysed all drug advertisements in the Ceylon Medical Journal (CMJ) 1985-1986. Conformity with the existing WHO guidelines and IFPMA code was also assessed. The 111 advertisements constituted 42% of the pages in the CMJ. Thirty-one of 34 companies were from the industrialized nations. Twenty-one per cent of the advertisements did not have the generic name; 94% had information on indications, whereas only 23 and 22% had information on adverse effects and contraindications. Only 16% provided information on generic name, indications, dosage, adverse effects and contraindications. Despite this 68% satisfied the criteria of the WHO guidelines and IFPMA code mainly under an ill defined 'reminder advertisement' clause. The existing guidelines are insufficient to ensure the minimum scientific information in drug advertisements.

Advertising↗
PubMed1988

Correction of systolic time intervals for heart rate: a comparison of individual with population derived regression equations.

1. We have examined the problem of how systolic time intervals (STI) should be corrected for heart rate in clinical pharmacological studies. 2. 'Individual' linear regression equations describing the relationship between STI and heart rate were derived for each of 43 healthy young adults (30 men and 13 women) by measuring STI at different heart rates produced by incremental doses of intravenous atropine. 'Population' equations for each sex were obtained by taking the mean of the 'individual' regression coefficients. 3. In order to assess which method more effectively reduced variability of the STI, 'individual' regression coefficients were derived for eight men who had previously participated in a placebo-controlled study which had used STI to test the cardiovascular effects of calcium antagonists alone and in combination with propranolol. 4. Within-subject variability in rate-corrected STI was similar after application of 'individual' and 'population' regression equations. Between-subject variability tended to be less after the use of 'population' equations. 5. 'Population' regression equations were more effective than 'individual' regression equations in allowing detection of differences between treatments, as judged by F values from ANOVA. 6. In clinical pharmacological studies including measurements of STI in healthy young subjects, 'individual' regression equations appear to have no advantage over 'population' equations derived in a group of subjects of similar age and sex.

Adult↗
PubMed1987

Alpha 2-adrenoceptor agonists stimulate growth hormone secretion but have no acute effects on plasma cortisol under basal conditions.

Ten normal male subjects were administered clonidine (0.1 and 0.2 mg) or a highly-selective alpha 2-adrenoceptor agonist S 3341 (1 and 2 mg) on separate occasions in a double-blind randomised placebo-controlled study; blood samples were obtained for measurement of serum GH and plasma cortisol via an indwelling venous cannula for 4 h after each drug administration. Both clonidine and S 3341 were equally effective at lowering supine, and particularly standing BP; both also caused mild sedation, although this was slightly less marked for S 3341. High doses of both clonidine and S 3341 significantly increased serum GH (peak increment after clonidine: 18.8 +/- 5.5 mU/l (mean +/- SEM); peak increment after S 3341: 21.1 +/- 4.8 mU/l). Neither drug affected plasma cortisol. It is concluded that GH release may be stimulated by alpha 2-adrenoceptor agonism. As S 3341 has slightly less central activity than clonidine at the doses employed, but is at least equally potent at stimulating GH release, it is probable that the alpha 2-adrenoceptor stimulation of GH release occurs outside the blood-brain barrier. The pituitary-adrenal axis appears resistant to manipulation of alpha 2-adrenoceptors under basal conditions.

Adrenergic alpha-Agonists↗
PubMed1984

Preliminary clinical pharmacological studies of S3341, a new hypotensive agent, and comparison with clonidine in normal males.

S3341, a new hypotensive agent which binds to alpha2-receptors in animal brain preparations, was studied in normal healthy male volunteers. A dose ranging study with 15 and 25 micrograms/kg of S3341 was performed in a double blind, placebo controlled randomised and balanced manner with 3 subjects. A decrease or BP without noticeable sedation (assessed by visual analogue scales) was seen. One, 2 mg of S3341, 0.1 and 0.2 mg of clonidine were then compared in a double blind, placebo controlled, randomised and balanced manner in 10 subjects. BP, heart rate, systolic time intervals (STI), critical flicker frequency, choice reaction time, pursuit rotor, stimulated salivary volume, and dryness of mouth and sedation with visual analogue scales, were measured at 0, 1.5, 3.0, 4.5 and 6.0 h after drug administration. The relationship between decreases in BP and sedation was assessed by linear regression analysis, with the former as the independent (predictor) response and the latter as the dependent (response) variate. Both drugs produced a similar decrease of BP which was significantly different from placebo. Changes in psychomotor function tests were not significant. Both drugs produced dryness of mouth and sedation which were significantly different from placebo but changes were less with S3341. Clonidine showed a significantly steeper slope than S3341 in the relationship between decreases in BP and sedation. This must be interpreted with caution as there was wide variation in the correlation between decreases in BP and sedation, but it may be possible to achieve lesser sedation with S3341.

Adrenergic alpha-Agonists↗
PubMed1982

Beta-adrenoceptor blockade and migraine.

Except for propranolol, no other Beta-blocker has been studied thoroughly in the prophylaxis of migraine. Of those studied, propranolol, atenolol and timolol were shown to be useful in double-blind clinical trials. The mode, or even the site of action of these drugs in unknown. Possible mechanisms of action are peripheral vascular effects, a central action, 5-HT antagonism, an anxiolytic effect and a multifactorial action. The only common property of the successful drugs is lack of partial agonist activity and their profiles do not fully support any of the above hypotheses. Trials of drugs in the prophylaxis of migraine have in general been unsatisfactory due to the difficulty in controlling many variables. Beta-blockers with differing properties offer an opportunity to define the properties necessary for anti-migraine activity and perhaps shed light on the pathogenesis of migraine.

Adrenergic beta-Antagonists↗