The airways response to phenylephrine after blockade of alpha and beta receptors in extrinsic bronchial asthma

Patel, K R; Kerr, J. W.

doi:10.1111/j.1365-2222.1973.tb01351.x

Cited by 56 publications

(20 citation statements)

References 19 publications

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“…Those agonists contract isolated bronchial smooth muscle [7,8], enhance in vitro secretion of airways submucosal glands [25], and facilitate histamine release from sensitized human lung tissue [26]. These effects probably account for the development of bronchial obstruction ascribed to stimulation of α 1 -adrenoceptors in some asthmatic subjects [7,[27][28][29]. They are also consistent with reported beneficial effects of various α 1 -adrenoceptor antagonists in asthma [30][31][32].…”

Section: Discussionsupporting

confidence: 74%

Effects of pretreatment with inhaled methoxamine on bronchial responses to histamine in asthmatic subjects

Phan-Puibaraud¹,

Regnard²,

Monchi³

et al. 1995

Eur Respir J

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The underlying mechanisms of bronchial obstruction in asthma are complex. Both bronchospasm and bronchial oedema are thought to play pivotal roles in asthma, but their respective importance in a given asthmatic individual is unknown. To address this question, we assessed the effects of pretreatment with inhaled methoxamine, a potent alpha 1-adrenoceptor agonist, on bronchial response to inhaled histamine in 10 asthmatic subjects. The study was conducted according to a double-blind, cross-over, randomized and placebo-controlled design. In each subject, dose-response curves for the effects on forced expiratory volume in one second (FEV1) of serially doubling doses of inhaled histamine were obtained on three different days, 15 min after pretreatment with either methoxamine (10 mg) or duplicated placebo. Histamine, first dose 100 micrograms (543 nmol), was delivered by a breath-activated dosimeter every 5 min. FEV1 was measured in triplicate after each dose and the largest value was retained. There was no difference in baseline and prechallenge FEV1 after placebo and methoxamine. Mean coefficient of variation of decrease in FEV1 induced by histamine on the two placebo days was 6.7 +/- 2%. On average, the bronchial responses to histamine were not modified by pretreatment with methoxamine as compared to placebo (delta FEV1 = 0.83 +/- 0.14 l on methoxamine versus 0.85 +/- 0.11 l and 0.86 +/- 0.13 l on the two placebo days).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 74%

Effects of pretreatment with inhaled methoxamine on bronchial responses to histamine in asthmatic subjects

Phan-Puibaraud¹,

Regnard²,

Monchi³

et al. 1995

Eur Respir J

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“…Lately, experiments conducted in vivo prove that clonidine intermediates an inhibitor control of the existing vagal activity. However, these results are not verified by other researchers [12]. Thomson et al [13] has proved that in the group of asthmatics, agonist of alpha-1 adrenergic receptor, inhaled phenilefrine does not affect the airway resistance.…”

Section: Introductioncontrasting

confidence: 52%

Adrenergic Agonist and Antagonist Action in Airways of Patients with Bronchial Asthma

Islami¹,

Krasniqi²,

Abdullahu³

2011

J Pulmonar Respirat Med

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In this study, the effect of dopamine as agonist dopaminergic receptor and alpha and beta adrenergic receptor was studied both in vivo. The effect of tolazoline as an antagonist of alpha-2 adrenergic receptor was also studied in patients with bronchial asthma and persons with increased bronchial reactibility. Parameters of the lung function are determined by body plethysmography. Raw and ITGV were registered and SRaw was calculated as well. Aerosolization is done with standard aerosolizing machines -Asema. Results gained in vivo shows that stimulation of alpha adrenergic receptor with dopamine (4 µg and 300 µg) causes significant contraction (p > 0.1) of the smooth bronchial musculature. Whereas, blockage of alpha-2 adrenergic receptor with tolazoline (20 mg by inhalator ways) does not change the bronchimotor tonus significantly (p>0.1) when compared to the stimulation of beta-2 adrenergic receptor with hexoprenaline (2 inh. x 0.2 mg) and blocker of cholinergic receptor -ipratropium (2 inh. x 1 mg). Reaction of the smooth musculature to dopamine suggests that this substance may cause constriction through alpha adrenergic receptors. Reaction may also be intermediated in indirect ways through dopaminergic receptor of the cholinergic transmission, with intracellular inhibition of the creation of cAMP.

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“…The existence of «-adrenergic receptors in bronchial asthma was assumed by several investigators, because catecholamines with a-and /(-sympathomimetic properties act as bronchoconstrictors when the /(-adrenergic receptors are blocked [de Kock, 1970;Si monsson et al, 1972;Prime et al, 1972;Patel and Kerr, 1973]. Bacterial endotoxin has been shown capable of potentiating this «-adrenergic activity [Simonsson et al, 1972].…”

Section: Discussionmentioning

confidence: 99%

“…De Kock [1970], Simonsson et al [1972], Prime et al [1972], and Patel and Kerr [1973] have shown that catechol amines like epinephrine or phenylephrine induce an increase of airway resistance in asthmatic patients when the ^-adrenergic system is blocked. This effect can be sup pressed by «-receptor blocking drugs.…”

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confidence: 99%

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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The airways response to phenylephrine after blockade of alpha and beta receptors in extrinsic bronchial asthma

Cited by 56 publications

References 19 publications

Effects of pretreatment with inhaled methoxamine on bronchial responses to histamine in asthmatic subjects

Effects of pretreatment with inhaled methoxamine on bronchial responses to histamine in asthmatic subjects

Adrenergic Agonist and Antagonist Action in Airways of Patients with Bronchial Asthma

Role of Alpha-Adrenergic Receptors in Exercise-Induced Bronchoconstriction

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