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Biomedical subjects

R G Shanks

Publications and source records attributed to R G Shanks.

At least 163 records · Page 9Linked to original sources
PubMed1970

Comparison of the effects of propranolol and MJ 1999 on cardiac beta-adrenoceptors in man.

1. Propranolol, a beta-adrenoceptor blocking drug with local anaesthetic and a direct myocardial depressant action, and MJ 1999, a beta-adrenoceptor blocking drug which has no local anaesthetic or intrinsic sympathomimetic action, were compared for beta-adrenoceptor blocking activity in man.2. Propranolol was 2.67 times more active than MJ 1999 in reducing by 50% the tachycardia produced by the intravenous infusion of isoprenaline in healthy volunteers.3. Propranolol and MJ 1999 intravenously both reduced resting heart rate in the standing position and an exercise tachycardia, but there was no qualitative or quantitative difference between them.4. On oral administration, both propranolol and MJ 1999 reduced resting heart rate and an exercise induced tachycardia; propranolol was only slightly more active than MJ 1999.5. In patients with thyrotoxicosis propranolol was about twice as active as MJ 1999 in reducing the heart rate.

Adrenergic beta-Antagonists↗
PubMed1969

The cardio-toxicity of isoprenaline during hypoxia.

1. The effects of the intravenous injection of isoprenaline on heart rate and arterial pressure has been studied in dogs artificially respired with room air or with 12% oxygen-88% nitrogen.2. In dogs breathing room air, isoprenaline in doses from 0.02 to 500 mug/kg increased heart rate and reduced arterial pressure. Ventricular fibrillation was produced in one out of three dogs given 250 mug/kg. This was the only dog breathing room air which was killed by isoprenaline.3. In dogs breathing room air the repeated intravenous injection at 5-min intervals of 2.5 mug/kg increased heart rate and reduced arterial pressure. No ill effects were produced by six doses.4. In dogs respired with 12% oxygen-88% nitrogen the PaO(2) was reduced from 84 to 38 mm Hg with no changes in PaCO(2). In these dogs death was produced by doses of isoprenaline which in dogs breathing room air produced normal responses.5. The fatal dose of isoprenaline (10-50 mug/kg) reduced heart rate and arterial and pulse pressures; sinus rhythm persisted until arterial pressure was less than 50 mm Hg. Ventricular fibrillation did not occur; death occurred from cardiac asystole.6. Death was produced in a similar way in dogs with hypoxaemia by giving four or five doses of isoprenaline (2.5 mug/kg) at 5-min intervals or by two doses of 25 mug/kg.7. The final reduction in arterial pressure during a fatal response resulted from a reduction in cardiac contractility.8. These lethal effects of isoprenaline could be prevented by pretreatment with propranolol.

Animals↗
PubMed1969

Inhibition of the carotid sinus reflex by the chronic administration of propranolol.

1. The changes in heart rate and arterial pressure produced by the intravenous injection of isoprenaline (0.5 mug/kg), noradrenaline (1.0 mug/kg), phenylethylamine (0.5 mg/kg), amphetamine (0.5 mg/kg) and by bilateral occlusion of the carotid arteries and by stimulation of the central ends of both vagus nerves have been recorded in groups of dogs anaesthetized with pentobarbitone.2. The acute intravenous injection of propranolol (1 mg/kg) reduced the increases in heart rate produced by the six procedures, the increases in arterial pressure in response to the last five procedures and the decrease in pressure produced by isoprenaline.3. This decrease produced by propranolol in the pressor responses resulted from a reduction in the increases in cardiac output elicited by the five procedures and has been attributed to blockade of cardiac adrenergic beta-receptors.4. Three groups of dogs were pretreated for 6 weeks by the oral administration of either placebo, propranolol 50 mg/kg daily or propranolol 10 mg/kg twice daily. The responses to the six test procedures were obtained 17-24 hr after the last dose of propranolol, when only minimal blockade of adrenergic beta-receptors was present. In the propranolol-treated groups, the pressor response to carotid occlusion but not to the other test procedures was significantly reduced.5. The pressor response to carotid occlusion was not reduced in a fourth group of dogs given a single dose of propranolol (50 mg/kg) 24 hr before the test procedures.6. The mechanism of this selective reduction in the pressor response to occlusion of the carotid arteries is not clear. It is suggested that it may contribute to the hypotensive action of propranolol in man during prolonged oral administration.

Amphetamine↗