The effects of ICI 118,587 and atenolol on the responses to exercise and on breathlessness in healthy subjects.

O'Neill, PA; Morton, P.B.; Sharman, Patrick; Marlow, HF; Stark, RD

doi:10.1111/j.1365-2125.1984.tb04996.x

Cited by 9 publications

(5 citation statements)

References 12 publications

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“…As has been stressed previously, this validation is an important part of studies examining the effects of drugs on breathlessness and has usually been an integral part of the experimental design O'Neill et al, 1984). In the present study, it has been shown that the validation can be performed at a single session.…”

Section: Discussionmentioning

confidence: 69%

Chlorpromazine‐a specific effect on breathlessness?

O'Neill¹,

Morton²,

Stark³

1985

Brit J Clinical Pharma

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Previous work has left unresolved questions on whether promethazine reduces the sensation of breathlessness. This study was designed to provide a definitive answer and to determine the contributions from promethazine's major pharmacological actions. Twelve healthy subjects participated in a double‐blind, within‐subject comparison of promethazine and placebo each given acutely by mouth. Breathlessness was assessed with visual analogue scales during a progressive exercise test and was related to minute ventilation. Promethazine had no significant effect on breathlessness nor on the relationship between breathlessness and ventilation. The role of histamine‐antagonism was investigated in a subgroup of the subjects by administration of mebhydrolin. No effect on breathlessness was detected. In contrast, the standard phenothiazine, chlorpromazine, caused a marked and statistically significant reduction in breathlessness without affecting ventilation and without causing detectable sedation. This unexpected finding merits further study in patients and is discussed with reference to the role of chlorpromazine as a constituent of Brompton's Mixture.

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Section: Discussionmentioning

confidence: 69%

Chlorpromazine‐a specific effect on breathlessness?

O'Neill¹,

Morton²,

Stark³

1985

Brit J Clinical Pharma

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“…The purpose of this study was to investigate the effects of xamoterol, a partial 1l-adrenoceptor agonist (Nuttall & Snow, 1982;Rousseau et al, 1983) on lung function, HR and BP in comparison with placebo and atenolol, a 1ladrenoceptor-selective antagonist (Ellis et al, 1981;Lammers et al, 1985). Xamoterol acts as a P-adrenoceptor agonist at low levels of sympathetic tone, but as a P-adrenoceptor antagonist when sympathetic tone is high, as during exercise (Harry et al, 1981;Rousseau et al, 1983;O'Neill et al, 1984). As we were interested to see whether xamoterol had any effect on lung function in view of its intrinsic sympathomimetic activity, the patients were studied at rest.…”

Section: Discussionmentioning

confidence: 99%

“…Xamoterol acts as a P-adrenoceptor agonist at low levels of sympathetic tone, but as a P-adrenoceptor antagonist when sympathetic tone is high, as during exercise (Harry et al, 1981;Rousseau et al, 1983;O'Neill et al, 1984). As we were interested to see whether xamoterol had any effect on lung function in view of its intrinsic sympathomimetic activity, the patients were studied at rest.…”

Section: Discussionmentioning

confidence: 99%

A comparative study on the ventilatory and haemodynamic effects of xamoterol and atenolol in asthmatic patients.

Lammers¹,

Müller²,

Folgering³

et al. 1986

Brit J Clinical Pharma

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1 The effects of single oral doses of atenolol 50 mg and xamoterol 200 mg ( a recently developed partial P1-adrenoceptor agonist) on lung function, heart rate and blood pressure were investigated in 11 patients with asthma. 2 Xamoterol caused a significant increase in heart rate and systolic blood pressure, which changes are consistent with the partial ,3l-adrenoceptor agonist activity of this drug.3 Atenolol induced a significant decrease in FEV1 and the forced vital capacity (FVC); there was a non-significant change in FEV1 and FVC after xamoterol. There was no significant difference between the effects of atenolol and xamoterol on FEV1 and FVC. 4 Bronchospasm induced by atenolol 50 mg and xamoterol 200 mg was completely reversed by inhalation of the P2-adrenoceptor agonist terbutaline to a cumulative dose of 4.0mg.

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“…Some support for a role for J receptors being involved in breathlessness during exercise in normal subjects emerged from a study of ~-adrenoceptors. An antagonist increased breathlessness during exercise and this could not be attributed to a change in bronchomotor tone [12). It is possible, that a reduction in cardiac contractility caused a rise in pulmonary capillary pressure with associated stimulation of J receptor activity.…”

Section: Interventions Affecting Respiratory Drives: Role Of the Vagusmentioning

confidence: 93%

Dyspnoea: assessment and pharmacological manipulation

Stark¹

1988

Eur Respir J

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A recent meeting of the European Society for Clinical Respiratory Physiology, held in Antwerp, focused on the mechanisms and management of respiratory symptoms. Dyspnoea received particular attention and this review is based on a talk presented at that meeting.The clinical problem posed by dyspnoea, or breathlessness, is of considerable magnitude. Precise data on its prevalence a re lacking but it is the most common symptom in patients with cardiorespiratory disease. Many chronic diseases are associated with dyspnoea, notably cardiac failure and chronic obstructive pulmonary disease. Extrapolation from the epidemiological survey of the Respiratory Diseas~ Study Group of the RCGP [I) would suggest that. m the UK alone, approximately 750,000 patients with chronic bronchitis experience dyspnoea induced by walking on level ground.A therapeutic agent which reduces the sensation of dyspnoea would be expected to improve the quality of life for the patient by delaying the restrictions on Hfestyle imposed by breathlessness and by mitigating a symptom which causes distress and induces anxiety. This would be no substitute for specific therapy directed at the underlying disease process, but could be of value when the patholot:,ry is not reversible. Close analogies exist with the use of analgesics to treat pain.Discovery of drugs to reduce dyspnoea is difficult because the pathophysiological mechanisms are still in dispute. In addition, animal models are limited in the study of sensations. In this laboratory known pharmacological agents were used in studies on man to discover the possible mechanisms of dyspnoea.No progress could be made until methods were available for assessing breathlessness. Precision was necessary in these assessments and there had to be knowledge of the reliability and limitations of the method in view of its subjective nature. Over about ten years, experience has been gained ~hich provi?es opportunities to optimize future experunentaJ des1gn and to appreciate when credibility has been over-

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The effects of ICI 118,587 and atenolol on the responses to exercise and on breathlessness in healthy subjects.

Cited by 9 publications

References 12 publications

Chlorpromazine‐a specific effect on breathlessness?

Chlorpromazine‐a specific effect on breathlessness?

A comparative study on the ventilatory and haemodynamic effects of xamoterol and atenolol in asthmatic patients.

Dyspnoea: assessment and pharmacological manipulation

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