Effects of beta-adrenergic blockade and stimulation on normal human airways.

Tattersfield, AE; Leaver, D. G.; Pride, N. B.

doi:10.1152/jappl.1973.35.5.613

Cited by 70 publications

(17 citation statements)

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“…Although the half-life of the drug is more than two hours in man (Paterson et al, 1970;Tattersfield et al, 1973), we observed a rapid disappearance of the bronchomotor effect of the betablockade in our subjects, the maximum being close to 5 minutes after the injection. That this effect is only transient remains unexplained, and could be due to a spontaneous reduction in vagal tone.…”

Section: Discussioncontrasting

confidence: 52%

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Beta-adrenergic function in airways of healthy and asthmatic subjects.

Gayrard¹,

Orehek²,

Grimaud³

et al. 1975

Thorax

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(1975). Thorax, 30,[657][658][659][660][661][662] Beta-adrenergic function in airways of healthy and asthmatic subjects. We measured the short-term effects of beta-adrenergic blockade with propranolol (0-2 mg/kg iv), followed by stimulation with salbutamol (200 ,ug inhaled), on specific airway conductance (SGaw), heart rate, and systemic blood pressure (BP) in 11 healthy subjects, and 11 symptom-free asthmatics with normal lung function values.Propranolol induced a significant bronchoconstrictor effect in both groups, stronger in asthmatics than in normals: mean SGaw decreased 34-6-4-25% against 9-4±+-9% (P<0-01). Six of the 11 asthmatics exhibited a more pronounced bronchoconstriction than the most responsive healthy subject. Large individual variations were seen in both groups although they were greater in the asthmatics. A similar rise in SGaw was produced by salbutamol in both groups. The decrease of heart rate provoked by propranolol was similar in the two groups, averaging 18-6%, with no further change after salbutamol. The blood pressure was slightly decreased by propranolol in both groups.The results indicate that normal subjects have a weak and variable bronchodilator beta-adrenergic activity. In most asthmatics beta-adrenergic tone appeared more pronounced. The individual differences in response to propranolol observed in both groups suggest that asthmatic patients differ quantitatively rather than qualitatively from healthy subjects with respect to beta-adrenergic receptor function. There was no association between clinical findings and the degree of bronchomotor effect of propranolol in the patients with asthma. This study does not support the view that airways of asthmatic patients have a decreased beta-adrenergic receptor function.

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Section: Discussioncontrasting

confidence: 52%

“…That this effect is only transient remains unexplained, and could be due to a spontaneous reduction in vagal tone. Such changes could have been missed in some other studies (Tattersfield et al, 1973).…”

Section: Discussionmentioning

confidence: 94%

Beta-adrenergic function in airways of healthy and asthmatic subjects.

Gayrard¹,

Orehek²,

Grimaud³

et al. 1975

Thorax

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“…Furthermore, electrical field studies [18][19][20][21] suggest that there is no functional sympathetic innervation of human airway smooth muscle, although adrenergic nerves may influence bronchomotor tone indirectly by a modulatory influence on cholinergic ganglionic neurotransmission [8]. Nevertheless, beta-adrenoreceptor antagonists have no effect on resting bronchomotor tone in normal humans [22,23]. In humans, the only direct neural bronchodilator pathway is provided by the nonadrenergic noncholinergic (NANC) innervation, which probably passes alongside the cholinergic nerves [7,24].…”

Section: Discussionmentioning

confidence: 99%

Thoracoscopic sympathicolysis for essential hyperhidrosis: effects on pulmonary function

Noppen¹,

Vincken²

1996

Eur Respir J

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Bilateral interruption of the upper dorsal sympathetic chain at the D2 and D3 level represents the only permanent cure for essential hyperhidrosis. Following surgical sympathectomy, significant and symptomatic changes in pulmonary function have been observed. Since functional effects of the surgical intervention cannot be excluded, we wondered whether such alterations also occurred after thoracoscopic sympathicolysis; these should then be attributable to the surgical denervation itself.Pulmonary function tests (PFTs), including spirometry and body plethysmographic measurement of lung volumes and airway resistance and conductance, were compared before and 6 weeks after thoracoscopic sympathicolysis in 47 patients. In order to virtually exclude any effects of thoracoscopy on the test results, PFTs were repeated 6 months after thoracoscopic sympathicolysis in 35 patients.Essential hyperhidrosis was completely relieved in all patients, thereby confirming the interruption of the D2-D3 sympathetic chain. None of the patients developed respiratory symptoms after thoracoscopic sympathicolysis. Forced expiratory volume in one second (FEV1) (-3%), forced expiratory flow after exhaling 75% of vital capacity (FEF75) (-8%) and total lung capacity (TLC) (-3%) were slightly but significantly reduced at six weeks after thoracoscopic sympathicolysis; whereas airway resistance (Raw) had increased (+12%). After correction for the small decrease in lung volume (FEV1/forced vital capacity (FVC), specific airway resistance (sRaw), specific airway conductance (sGaw))significant changes in "volume-dependent" PFT parameters were no longer observed. Smoking status had no influence on the reduction in FEF75. At 6 months after thoracoscopic sympathicolysis, TLC had returned to preoperative values, whereas FEF75 remained decreased (-8.6%). The decrease in airway calibre was confirmed by small but significant changes in FEV1/FVC (-2%) and Raw (+29%).We conclude that thoracoscopic sympathicolysis in patients with essential hyperhidrosis causes only minimal and subclinical changes in pulmonary function secondary to a temporary small decrease in lung volume, which in turn is probably inherent to the thoracoscopic procedure. D2-D3 sympathicolysis, in itself, is responsible only for a small and permanent decrease in forced expiratory flow, which suggests that, at least in essential hyperhidrosis patients, airway bronchomotor tone is influenced by sympathetic innervation. Eur Respir J., 1996Respir J., , 9, 1660Respir J., -1664 Essential hyperhidrosis (EH) is a disorder characterized by excessive sweating of the palms of the hands and often the armpits and soles of the feet [1]. It is caused by a poorly understood overactivity of the sympathetic nervous system at the level of the D2 and D3 dorsal sympathetic ganglia [2]. Anatomical interruption of the sympathetic innervation at this level, preferably by minimally invasive techniques, such as percutaneous ablation or thoracoscopy, provides a permanent cure in patients with severe EH refr...

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“…The full inflation preceding the forced expiration might remove the bronchomotor tone present during tidal breathing since bronchoconstriction induced by histamine and other agents in normal subjects is generally agreed to be removed for some seconds by a full inflation. It is less certain that normal tone is removed (Nadel & Tierney, 1961 ;Tattersfield, Leaver & Pride, 1973 (Figure 3). Also the earliest changes may be in the tail of the expiration, so that a characteristic convexity of the MEFV curve towards the volume axis develops with Vmax25 changing proportionately more than Vmax50 or PEF.…”

Section: Normal Subjectsmentioning

confidence: 99%

Assessment of changes in airway calibre I. Tests of forced expiration.

Pride¹

1979

Brit J Clinical Pharma

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Effects of beta-adrenergic blockade and stimulation on normal human airways.

Cited by 70 publications

References 0 publications

Beta-adrenergic function in airways of healthy and asthmatic subjects.

Beta-adrenergic function in airways of healthy and asthmatic subjects.

Thoracoscopic sympathicolysis for essential hyperhidrosis: effects on pulmonary function

Assessment of changes in airway calibre I. Tests of forced expiration.

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