PubMed Health⌕ Search

Biomedical subjects

C A Haffner

Publications and source records attributed to C A Haffner.

9 recordsLinked to original sources
PubMed1992

Metabolic effects of beta 2-agonists.

Catecholamines produce a number of biochemical changes most of which result from stimulation of beta 2-receptors. Interest in these metabolic effects has increased recently as a consequence of the concern over the relatively high mortality from acute asthma attacks. In this review the data on the impact of beta 2-agonists on glucose production, insulin release and lipolysis are presented. Thereafter the subject of hypokalaemia, the mechanism for its production by beta 2-agonists and its relevance to cardiac arrhythmias are considered in detail. Finally the fall in plasma magnesium and the possible role of beta 2-agonists in the production of lactic acidosis are discussed.

Acidosis, Lactic↗
PubMed1992

Pilot study to compare the bronchodilator and metabolic responses to terbutaline infusion in seven asthmatic subjects--are they correlated?

We compared the changes in peak expiratory flow rate (PEFR), plasma potassium and plasma glucose during and after an infusion of the beta 2-agonist, terbutaline, in seven asthmatic subjects. Our aim was to establish whether these metabolic parameters could be correlated with PEFR. The percentage changes in PEFR were significantly correlated with the percentage changes in glucose (r = 0.60, P less than 0.001) and potassium (r = -0.64, P less than 0.001). Values for glucose and potassium changes were also correlated significantly with each other (r = 0.86, P less than 0.001). This suggests that in asthmatic subjects on beta 2-agonist treatment, plasma potassium could be used as a surrogate marker for beta 2 activity at bronchi. It also implies that the most effective beta 2-agonist bronchodilators will produce the greatest fall in plasma potassium. Further studies with a larger number of patients are needed to confirm this.

Adult↗
PubMed1992

A metabolic assessment of the beta 1 selectivity of bisoprolol.

Twelve healthy volunteers were given single oral doses of bisoprolol 5 mg, 10 mg and 20 mg and atenolol 50 mg and 100 mg in a randomised, placebo-controlled study. The effects of these drugs on beta 2-stimulated hypokalaemia and hyperglycaemia (produced by intravenous terbutaline infusion) were studied. Comparable beta-blockade was achieved with bisoprolol 20 mg, and atenolol 50 mg and 100 mg as measured by attenuation of exercise heart rate. Measurements of areas under or over the curve (AUC and AOC) of hypokalaemic or hyperglycaemic response to terbutaline infusion showed that bisoprolol (10 mg and 20 mg) and atenolol (50 mg and 100 mg) were significantly less beta 1 selective than 5 mg bisoprolol. Furthermore, there was a trend towards decreasing beta 1 selectivity with increasing doses of bisoprolol. Bisoprolol, an effective once daily antihypertensive and antianginal treatment, has comparable beta 1 selectivity to atenolol as measured by metabolic response. At a dose of 5 mg, bisoprolol has a measurable impact on beta 1 receptors but minimal effect on beta 2 receptors.

Adrenergic beta-Antagonists↗
PubMed1991

Assessment of beta-1 selectivity of bisoprolol and atenolol by means of their influence on the lipolytic response to an infusion of terbutaline.

We have investigated the beta-1 selectivity of a new beta-blocker, Bisoprolol, by comparing its effect on lipolysis induced by intravenous terbutaline infusion with that of Atenolol. At a dose of 5 mg, Bisoprolol had virtually no beta-2 blocking activity as measured by free fatty acid (FFA) release during terbutaline infusion. At a dose of 10 mg, Bisoprolol had a small but statistically insignificant effect on FFA release similar to 50 mg Atenolol. At a dose of 20 mg, Bisoprolol had significant beta-2 blocking activity. At lower doses, therefore, Bisoprolol is a very selective beta-blocker.

Adrenergic beta-Antagonists↗
PubMed1991

Investigation of the effects of beta-2 stimulation on free fatty acids in man.

In this study we present evidence that lipolysis in man is under beta-2 adrenergic control and that beta-2 stimulation produces a characteristic profile of individual free fatty acid (FFA) release. Twelve healthy volunteers received infusions of placebo (N Saline), terbutaline (a selective beta-2 agonist) and dilevalol (a new non-selective beta-blocker with beta-2 agonist activity). Plasma FFA concentrations during and after the infusions were measured using gas chromatography. A significant rise in total and individual FFAs was seen after 30 min of terbutaline infusion. This was most marked for oleic acid. Total and individual FFA concentrations also rose after 30 min of dilevalol infusion; this was only significant for oleic acid and was approximately 15% of the rise induced by terbutaline infusion. Placebo infusion did not cause any significant changes in FFA levels.

Adult↗
PubMed1990

Embryo research.

Explore the source record for details and available documents.

Abortion, Legal↗
PubMed1990

Investigation of the beta 2-agonist properties of dilevalol: metabolic effects of intravenous infusion.

We describe two studies which investigate the beta 2-agonist properties of dilevalol. We have previously demonstrated, by giving an infusion of terbutaline to human volunteers, that beta 2-stimulation causes a rise in plasma glucose and a fall in plasma potassium. These metabolic effects can be prevented by prior beta-blockade. We now show that infusion of dilevalol produces similar, but quantitatively smaller, metabolic effects at a dose which also produces clinically significant beta-blockade, as judged by a fall in exercise heart rate. This adds support to the claim that dilevalol is a non-selective beta-blocker with selective beta 2-agonist activity.

Adult↗