Drugs online research references
Scott Med J. 1977 Jan;22(1):69-72.
Observations in man of hypoglycaemia during selective and non-selective beta-blockade.
Davidson NM, Corrall RJ, Shaw TR, French EB.
The acute hypoglycaemic reaction is accompanied by a rise in systolic and a slight fall in diastolic blood pressure and a tachycardia. In contrast, during beta-blockade with propranolol there is a rise of both systolic and diastolic blood pressures and bradycardia. Restoration of blood glucose to normal is delayed. With metoprolol there is a lesser increase in diastolic blood pressure and a slight tachycardia. Restoration of the blood glucose to normal is little delayed. When patients liable to hypoglycaemia require a beta-blocking agent, it is suggested that a selective blocker such as metoprolol should be used.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=13497&dopt=Abstract
Indian J Physiol Pharmacol. 1978 Jan-Mar;22(1):61-5.
Enhancement of insulin hypoglycaemia by beta adrenoceptor antagonists.
Singh RC, Srivastava VK, Tayal G, Srivastava RK, Prasad DN.
Interaction of insulin with beta-adrenoceptor antagonists was studied in conscious rabbits. Propranolol and metoprolol did not modify the peak of insulin hypoglycaemia but delayed its recovery. Practolol, sotalol and 1-INPEA enhanced the peak effect and delayed the recovery of insulin-induced hypoglycaemia. H 35/25 and d-INPEA did not modify insulin hypoglycaemia. The beta-blockers did not produce significant hypoglycaemia per se. Since sotalol, 1-INPEA (specific beta-adrenoceptor antagonists devoid of local anaesthetic activity); practolol and metoprolol (selective cardiac beta-1 adrenoceptor antagonists) enhanced hypoglycaemic action of insulin and H 35/25 (a selective beta-2 adrenoceptor antagonist) failed to affect it, it seems that selective beta-adrenoceptor blockade (similar to cardiac beta-1 adrenoceptors) mediates enhancement of insulin hypoglycaemia. Caution should, therefore, be exercised in administering beta-adrenoceptor antagonists and insulin together. A reduction in the dose of insulin may be necessary.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=28289&dopt=Abstract
Acta Med Scand Suppl. 1983;672:63-7.
Adrenergic blockade and hypoglycaemia.
Lager I.
The metabolic effects of beta-adrenoceptor blocking agents during hypoglycaemia in patients prone to hypoglycaemia are of interest as diabetics are often treated with these drugs because of hypertension or angina pectoris. Compared with non-diabetics these patients also have impaired glucose compensation after hypoglycaemia, partly secondary to deficient release of glucagon. This makes the diabetics more dependent on adrenergic mechanisms to recover from low blood glucose concentrations. Non-selective beta-adrenoceptor blockade (propranolol) significantly impairs the glucose recovery rate after hypoglycaemia in insulin dependent diabetics, whereas selective beta-adrenoceptor blockade (metoprolol) does not have this side effect. The mechanism of the effect of propranolol is probably an attenuation of the gluconeogenesis secondary to deficient release of the important gluconeogenic substrates lactate and glycerol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6138936&dopt=Abstract
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