Sequential Estimation of Plasma Catecholamines in Exercise-Induced Asthma

Griffiths, John C.; Leung, F Y; Grzybowski, Stefan; Chan‐Yeung, Moira

doi:10.1378/chest.62.5.527

Cited by 30 publications

(8 citation statements)

References 17 publications

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“…[1972] and Bianco et al [1974] proposed that if there were a considerable number of «-adre nergic receptors in the bronchial tree in asthmatic patients, the «-adrenergic proper ties of increased circulating plasma catechol amine levels might prevail, but it is still unknown whether the sympathetic nervous system or the circulating catecholamines are of greater importance in bronchomuscular control [Widdicombe and Sterling, 1970], In normal persons, /¡-adrenergic block ade did not provoke any measurable EIB ( fig. 1), even though the circulating catechol amines, especially norepinephrine, increase relatively more in such cases during exercise than is the case in subjects without /2-block ade [Irving et al, 1974], But these observa tions do not negate the concept of Griffiths et al [1972] and Bianco et al [1974] of the pathogenesis of bronchoconstriction when it is remembered that normals are thought to have few, if any, «-receptors.…”

Section: Discussionmentioning

confidence: 96%

Role of Alpha-Adrenergic Receptors in Exercise-Induced Bronchoconstriction

Beil¹,

Kock²

1978

Respiration

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The role of α-adrenergic receptors in exercise-induced bronchoconstriction (EIB) was studied. 9 asthmatic patients with a marked degree of EIB (group I) and 6 asthmatic patients with no or a less severe EIB (group II) were investigated and compared with 8 healthy control persons. Pulse rate, airway resistance and end-expiratory thoracic gas volume were measured at rest and immediately and 15 min after exercise. Group I subjects showed a significant inhibition of EIB after α-adrenergic blockade with phentolamine (10 mg as aerosol) and after cholinergic blockade with an atropine-ester (60 mg as aerosol). In 7 of 9 patients who had received phentolamine, and in 3 of 6 patients who had received atropine-ester, the EIB was completely suppressed. In group II the administration of propranolol (40 mg orally) produced a significant increase in EIB. The effect of propranolol could be inhibited by the addition of α-adrenergic blockade with phentolamine (10 mg as aerosol). The control subjects had no measurable EIB, even after the administration of propranolol (40 mg orally). It is concluded that, in addition to the vagal system, an activated α-adrenergic system is involved in the phenomenon of EIB.

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Section: Discussionmentioning

confidence: 96%

Role of Alpha-Adrenergic Receptors in Exercise-Induced Bronchoconstriction

Beil¹,

Kock²

1978

Respiration

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“…Hypokalaemia predisposes to cardiac arrhythmias, however, none were observed in our young healthy subjects. In asthmatic or bronchitic patients there is conflicting evidence as to circulating adrenaline levels (Barnes et al, 1981;Griffiths et al, 1972;Zielinske et al, 1980;Chryssanthopoulus et al, 1978;Ind et al, 1985). However, co-existent hypoxia, acidosis or cardiovascular disease may increase the likelihood of salbutamol inducing arrhythmias in these patients.…”

Section: Discussionmentioning

confidence: 99%

The mechanism of salbutamol‐induced hypokalaemia.

Whyte

Addis

Whitesmith

et al. 1987

Brit J Clinical Pharma

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The following four intravenous treatments were administered in a balanced, randomized Latin square design to eight healthy volunteers: (‐)‐adrenaline (0.06 microgram kg‐1 min‐1 for 90 min) + vehicle control (+)‐glucose infusion (60 min), salbutamol (120 ng kg‐1 min‐1 for 30 min) + vehicle control (+)‐glucose infusion (90 min), (‐)‐adrenaline (0.06 microgram kg‐1 min‐1 for 90 min) + salbutamol (120 ng kg‐1 min‐1 for 30 min) and two vehicle control infusions of (+)‐glucose. All active solutions were preceded by a 1 h control infusion and the control infusion was continued for 1 h following the active solutions. Both the active solutions, (‐)‐adrenaline and salbutamol were increased stepwise to the above doses. Heart rate and blood pressure were recorded at frequent intervals throughout and venous blood was taken for the estimation of potassium, insulin, glucose, catecholamine and salbutamol levels. Adrenaline levels similar to those seen in acute illness were achieved using this infusion protocol. Salbutamol levels rose throughout the period of the salbutamol infusions and steady‐state was not achieved. Potassium levels were unchanged on the control + control study day and fell on all active treatments (0.45 mmol l‐1 following (‐)‐adrenaline + control; 0.48 mmol l‐1 following salbutamol + control; 0.93 mmol l‐1 following (‐)‐adrenaline + salbutamol). Insulin levels rose insignificantly after salbutamol alone and fell slightly on all other treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…In this study we have examined the changes in serum potassium and haemodynamics following the addition of therapeutic doses of theophylline to conventional doses of salbutamol. Circulating (-)-adrenaline concentrations may be raised in asthma, although the literature is conflicting (Ind etal., 1985;Barnes etal., 1981;Griffiths et al, 1972;Zielinske et al, 1980). Therefore we have also examined the effect of raising circulating (-)-adrenaline concentrations on the hypokalaemia induced by salbutamol in combination with theophylline.…”

Section: Introductionmentioning

confidence: 99%

Salbutamol induced hypokalaemia: the effect of theophylline alone and in combination with adrenaline.

Whyte

Reid

Addis

et al. 1988

Brit J Clinical Pharma

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1 We have previously shown that salbutamol induced hypokalaemia, like adrenaline induced hypokalaemia, is the result of stimulation of a membrane bound 132-adrenoreceptor linked to Na+/K+ ATPase. We have also demonstrated that adrenaline induced hypokalaemia is potentiated by therapeutic concentrations of theophylline. 2 In a single-blind study of 14 normal volunteers, we infused salbutamol in doses used in clinical practice and examined the effects of the addition of theophylline alone or combined with (-)-adrenaline on plasma potassium levels, heart rate and blood pressure. The combinations studied were (i) salbutamol + vehicle control adrenaline infusion + placebo theophylline; (ii) salbutamol + vehicle control adrenaline infusion + theophylline; (iii) salbutamol + adrenaline + theophylline. 3 In a randomised, balanced placebo controlled design oral slow release theophylline or placebo was given for 9 days. Subjects were studied twice on the active limb (days 7 and 9) and once on the placebo limb (day 9) and the procedure was identical on each of the 3 study days except for the solutions administered. 4 Theophylline increased salbutamol induced hypokalaemia and in some individuals profound hypokalaemia (< 2.5 mmol 1-1) was observed with these relatively low doses of salbutamol and theophylline. Adrenaline did not further increase the magnitude of the fall in potassium observed. Combining theophylline with salbutamol increased the tachycardia resulting from the salbutamol infusion. Salbutamol infusion caused a fall in diastolic and rise in systolic blood pressure on all 3 study days and this was not altered by either theophylline or adrenaline alone or together. 5 We conclude that theophylline significantly increases salbutamol induced hypokalaemia and tachycardia and that the addition of adrenaline does not further increase hypokalaemia. Intensive bronchodilator therapy with these two agents in acutely ill, hypoxic patients with asthma or chronic obstructive lung disease may increase the risk of serious cardiac arrhythmias secondary to hypokalaemia.

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Sequential Estimation of Plasma Catecholamines in Exercise-Induced Asthma

Cited by 30 publications

References 17 publications

Role of Alpha-Adrenergic Receptors in Exercise-Induced Bronchoconstriction

Role of Alpha-Adrenergic Receptors in Exercise-Induced Bronchoconstriction

The mechanism of salbutamol‐induced hypokalaemia.

Salbutamol induced hypokalaemia: the effect of theophylline alone and in combination with adrenaline.

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