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Biomedical subjects

D J Coltart

Publications and source records attributed to D J Coltart.

154 records · Page 9Linked to original sources
PubMed1970

Hypertrophic cardiomyopathy. An electrophysiological study.

Recordings of the transmembrane action potential of the cardiac myofibril from a patient with hypertrophic obstructive cardiomyopathy showed that the repolarization time was appreciably prolonged and that the maximum rate of follow was grossly reduced. This electrical abnormality is compatible with the late and irregular activation of the ventricular muscle in the disease. Propranolol was found to produce a similar "quinidine-like" effect on the transmembrane actionpotential in both cardiomyopathic and control tissue.

Action Potentials↗
PubMed1970

Plasma propranolol levels in the quaniitative assessment of beta-adrenergic blockade in man.

Plasma propranolol levels associated with reductions in endogenous and exogenous cardiac beta-stimulation were determined in normal people. The levels associated with a given degree of blockade of exercise-induced tachycardia were about three times greater after intravenous administration than after oral administration. This shows that an active metabolite of propranolol is formed only after the drug is taken by mouth. The greatest reduction in the tachycardia of strenuous exercise was associated with plasma levels of 40 ng./ml. with oral administration and 100 ng./ml. with intravenously administered propranolol.The effect on isoprenaline-induced tachycardia following intravenously administered propranolol showed that the dose ratio for isoprenaline was about 30 with plasma levels of 100 ng./ml. and 10 with levels of 10-20 ng./ml. These plasma levels give 100% and 20-30% blockade of exercise-induced tachycardia. These findings suggest that some of the therapeutic effects of propranolol may be unrelated to beta-adrenergic blockade.

Administration, Oral↗
PubMedDate not supplied

Effect of chronic beta-blockade on the ischaemic myocardium: a comparative study with five drugs.

The long-term effects of chronic beta-blockade in the rat myocardium were investigated in terms of responses to ischaemic stress. Clinically relevant and equipotent doses of oxprenolol, propranolol, metoprolol, atenolol, and practolol were administered orally for 12 weeks. Twenty-four hours after the last dose, at a time when plasma drug levels were undetectable, hearts were excised and perfused as isolated preparations. During a 3-h period of low-flow, global ischaemia, the time to electromechanical failure following the onset of ischaemia was significantly increased in hearts from animals treated with drugs possessing intrinsic sympathomimetic activity (ISA). Similarly, with ischaemia-induced lactate and enzyme release, hearts from groups treated with drugs possessing ISA showed an increase in release above that of controls, or of hearts from rats treated with beta-blockers which did not possess ISA. These results suggest that in the isolated, globally ischaemic heart, when exogenous catecholamine drive is absent, long-term beta-blockade cannot exert a protective effect when circulating drug levels are undetectable, and compounds possessing ISA may increase tissue damage as measured by lactate and enzyme leakage.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Diltiazem hydrochloride.

Since their introduction in 1963, calcium-channel blockers, with their effectiveness and lack of side effects, have become widely used. Diltiazem hydrochloride, a benzothiazine, has its major role in the treatment of angina and is also used as an antihypertensive and antiarrhythmic.

Angina Pectoris↗