Bronchoconstriction following inhaled ethanol solutions

Hooper, G. H. S.; Steed, K.P.; Gittins, D.P.; Newman, Steven P.; Richards, Anthony; Rubin, I.C.

doi:10.1016/0954-6111(95)90221-x

Cited by 8 publications

(5 citation statements)

References 4 publications

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“…Compared to nebulized saline, nebulized alcohol triggered coughing and caused a small but significant reduction in airflow that persisted for 90 minutes in all subjects, consistent with an irritant effect. This was anecdotally confirmed in case reports of two mild asthmatics who developed bronchospasm following exposure to 20% aerosolized ethanol alone as part of a drug safety protocol (Hooper et al, 1995). These authors concluded that the use of ethanol as a carrier for inhaled drug formulations is unpredictable and potentially hazardous in asthmatics (Hooper et al, 1995).…”

Section: Clinical Studies Of Alcohol and Asthmamentioning

confidence: 80%

“…This was anecdotally confirmed in case reports of two mild asthmatics who developed bronchospasm following exposure to 20% aerosolized ethanol alone as part of a drug safety protocol (Hooper et al, 1995). These authors concluded that the use of ethanol as a carrier for inhaled drug formulations is unpredictable and potentially hazardous in asthmatics (Hooper et al, 1995). This is also potentially important because of the rapidly increasing production and use of ethanol as a fuel additive.…”

Section: Clinical Studies Of Alcohol and Asthmamentioning

confidence: 81%

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Alcohol and airways function in health and disease

Sisson

2007

Alcohol

136

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The volatility of alcohol promotes the movement of alcohol from the bronchial circulation across the airway epithelium and into the conducting airways of the lung. The exposure of the airways through this route likely accounts for many of the biologic effects of alcohol on lung airway functions. The impact of alcohol on lung airway functions is dependent on the concentration, duration and route of exposure. Brief exposure to mild concentrations of alcohol may enhance mucociliary clearance, stimulates bronchodilation and probably attenuates the airway inflammation and injury observed in asthma and COPD. Prolonged and heavy exposure to alcohol impairs mucociliary clearance, may complicate asthma management and likely worsens outcomes including lung function and mortality in COPD patients. Non-alcohol congeners and alcohol metabolites act as triggers for airway disease exacerbations especially in atopic asthmatics and in Asian populations who have a reduced capacity to metabolize alcohol. Research focused on the mechanisms of alcohol-mediated changes in airway functions has identified specific mechanisms that mediate alcohol effects within the lung airways. These include prominent roles for the second messengers calcium and nitric oxide, regulatory kinases including PKG and PKA, alcohol and acetaldehyde-metabolizing enzymes such as aldehyde dehydrogenase type 2 (ALDH2). The role alcohol may play in the pathobiology of airway mucus, bronchial blood flow, airway smooth muscle regulation and the interaction with other airway exposure agents, such as cigarette smoke, represent opportunities for future investigation.

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Section: Clinical Studies Of Alcohol and Asthmamentioning

confidence: 80%

Section: Clinical Studies Of Alcohol and Asthmamentioning

confidence: 81%

Alcohol and airways function in health and disease

Sisson

2007

Alcohol

136

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“…A small but statistically significant increase in Penh in response to ethanol vehicle was seen in most lines tested. Variable effects of ethanol on airway tone have been reported in different species including humans (10,13,17,28). PGE 2 had no effect above that seen with vehicle alone in 129X1/Sv, 129SvEV, and DBA/2 mice.…”

Section: Effect Of Pge 2 On the Airways Of Conscious Micementioning

confidence: 87%

Receptors and pathways mediating the effects of prostaglandin E₂ on airway tone

Tilley

Hartney

Erikson

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

124

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(PGE2) has complex effects on airway tone, and the existence of four PGE2 [E-prostanoid (EP)] receptors, each with distinct signaling characteristics, has provided a possible explanation for the seemingly contradictory actions of this lipid mediator. To identify the receptors mediating the actions of PGE2 on bronchomotor tone, we examined its effects on the airways of wild-type and EP receptor-deficient mice. In conscious mice the administration of PGE2 increased airway responsiveness primarily through the EP1 receptor, although on certain genetic backgrounds a contribution of the EP3 receptor was detected. These effects of PGE2 were eliminated by pretreatment with either atropine or bupivacaine and were undetectable in anesthetized mice or in denervated tracheal rings, where only EP2-mediated relaxation of airway smooth muscle was observed. Together, our findings are consistent with a model in which PGE2 modulates airway tone by activating multiple receptors expressed on various cell populations and in which the relative contribution of these receptors might depend on the expression of modifier alleles. PGE2/EP1/EP3-induced airway constriction occurs indirectly through activation of neural pathways, whereas PGE2-induced bronchodilation results from direct activation of EP2 receptors on airway smooth muscle. This segregation of EP receptor function within the airway suggests that PGE2 analogs that selectively activate the EP2 receptor without activating the EP1/EP3 receptors might prove useful in the treatment of asthma. PGE2 receptor; bronchoconstriction; bronchodilation; knockout; nerves SHORTLY AFTER ITS DISCOVERY in the 1960s, prostaglandin E 2 (PGE 2 ) was observed to have potent relaxant effects on airway smooth muscle, making this endogenous lipid an attractive candidate drug for asthma (18,34). However, human studies with aerosolized PGE 2 have demonstrated inconsistent effects on airway tone, with most asthmatics showing a bronchodilator response but some developing profound bronchoconstriction requiring beta agonist rescue (6,19). Ex vivo studies from humans and animals have also shown that PGE 2 can both relax and constrict airway smooth muscle, a paradox explained when it was recognized that PGE 2 could act through more than one receptor (9,20,26).Four distinct cell surface receptors for PGE 2 [E-prostanoid (EP)] have been identified and cloned, each with unique signal transduction mechanisms as a result of coupling to different G proteins (23). Activation of one or a combination of receptors, each which may be differentially expressed on airway smooth muscle, epithelia, neurons, and immune effector cells, results in a specific physiological response. EP2 and EP4 receptors couple to G s , and activation of these receptors results in stimulation of adenylyl cyclase and increases in intracellular cAMP. Various EP3 isoforms, arising from the differential splicing of the EP3 gene, have been identified both in humans and in mice (1,24). Differences in the cytoplasmic domain of the EP3 receptor leads to th...

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“…Ayres, Ancic, & Clark, 1982) or taken intravenously (J. G. Ayres & Clark, 1983), even though it may provoke bronchospasm when inhaled (Hooper et al, 1995; Zuskin, Bouhuys, & Saric, 1981). However, in our study we found the strongest effects of alcohol intake on FVC, not FEV 1 .…”

Section: Discussionmentioning

confidence: 99%

Persistent light to moderate alcohol intake and lung function: A longitudinal study

Vasquez

Sherrill

LeVan

et al. 2018

Alcohol

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Alcohol intake has been inconsistently associated with lung function levels in cross-sectional studies. The goal of our study was to determine whether longitudinally assessed light-to-moderate alcohol intake is associated with levels and decline of lung function. We examined data from 1333 adult participants in the population-based Tucson Epidemiological Study of Airway Obstructive Disease. Alcohol intake was assessed with four surveys between 1972 and 1992. Subjects who completed at least two surveys were classified into longitudinal drinking categories ("never", "inconsistent", or "persistent drinker"). Spirometric lung function was measured in up to 11 surveys between 1972 and 1992. Random coefficient models were used to test for differences in lung function by drinking categories. After adjustment for sex, age, height, education, BMI categories, smoking status, and pack-years, as compared to never-drinkers, persistent drinkers had higher FVC (coefficient: 157 mL, p < 0.001), but lower FEV/FVC ratio (-2.3%, p < 0.001). Differences were due to a slower decline of FVC among persistent than among never-drinkers (p = 0.003), and these trends were present independent of smoking status. Inconsistent drinking showed similar, but weaker associations. After adjustment for potential confounders, light-to-moderate alcohol consumption was associated with a significantly decreased rate of FVC decline over adult life.

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Bronchoconstriction following inhaled ethanol solutions

Cited by 8 publications

References 4 publications

Alcohol and airways function in health and disease

Alcohol and airways function in health and disease

Receptors and pathways mediating the effects of prostaglandin E₂ on airway tone

Persistent light to moderate alcohol intake and lung function: A longitudinal study

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Bronchoconstriction following inhaled ethanol solutions

Cited by 8 publications

References 4 publications

Alcohol and airways function in health and disease

Alcohol and airways function in health and disease

Receptors and pathways mediating the effects of prostaglandin E2 on airway tone

Persistent light to moderate alcohol intake and lung function: A longitudinal study

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Product

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Receptors and pathways mediating the effects of prostaglandin E₂ on airway tone