Sensory neuropeptide-mediated bronchoconstriction of the guinea pig lung by diamide; a comparison to hydrogen peroxide

Bannenberg, Gerard; Kimland, Monika; Ryrfeldt, Åke; Lundberg, Jan M.; Moldéus, Peter

doi:10.1016/0926-6917(94)90060-4

Cited by 2 publications

(2 citation statements)

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“…Thus this mechanism is questionable, at least in the case of responses to 0.2% H 2 O 2 challenge. Unlike lung C fibers, RARs can be mechanically activated by several factors, including bronchoconstriction and changes in lung mechanics (8,39,51), results that may also be induced by H 2 O 2 (1).…”

Section: Discussionmentioning

confidence: 99%

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

Ruan

Kou

2003

Journal of Applied Physiology

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vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats. J Appl Physiol 94: 1987, 2003. First published January 10, 2003 10.1152/ japplphysiol.01047.2002We investigated the afferent vagal pathways mediating respiratory reflexes evoked by reactive oxygen species (ROS) in the lungs of anesthetized rats. Spontaneous inhalation of 0.2% aerosolized H 2O2 acutely evoked initial bradypnea followed by delayed tachypnea, which was frequently mixed with delayed augmented inspiration. The initial response was abolished after perivagal capsaicin treatment (PCT), but was prolonged during vagal cooling (VC) to 7°C; PCT and VC are known to differentially block the conduction of unmyelinated C and myelinated fibers, respectively. The delayed responses were eliminated during VC but emerged earlier after PCT. Vagotomy, catalase (an antioxidant for H 2O2), dimethylthiourea (an antioxidant for ⅐ OH), or deferoxamine (an antioxidant for ⅐ OH) largely or totally suppressed these reflexive responses, whereas sham nerve treatment, heat-inactivated catalase, saline vehicle, or iron-saturated deferoxamine failed to do so. These results suggest that 1) the H 2O2-evoked initial and delayed airway reflexes are antagonistic and may result from stimulation of lung C fibers and rapidly adapting receptors, respectively, and 2) the reflex effects of H 2O2 are, in part, due to the action of ⅐ OH on these afferents. vagal sensory receptors; oxygen radicals; reactive oxygen species; hydrogen peroxide LUNG DISEASES, SUCH AS ASTHMA (10), chronic obstructive pulmonary disease (12), endotoxin shock (33), and vascular microembolism (50), or inhalation of oxidant irritants, such as toxic smoke (35), cigarette smoke (35), and ozone (45), may cause increased pulmonary production of reactive oxygen species from endogenous and/or exogenous sources. The major reactive oxygen species are the superoxide anion radical, hydrogen peroxide (H 2 O 2 ), and the hydroxyl radical (⅐ OH) (5). The superoxide anion radical dismutates to form H 2 O 2 , which, in the presence of iron, can further react to form ⅐ OH, a more reactive oxygen radical, via the Fenton reaction (5). Vagal sensory receptors are known to play an important role in detecting the onset of pathophysiological conditions and are responsible for triggering defensive or protective airway reflexes (8, 29, 39).While abundant information suggests the importance of reactive oxygen species in producing pulmonary pathophysiological consequences (4), very few studies have investigated their role and mechanism in eliciting airway reflexes.The concept that reactive oxygen species may stimulate pulmonary sensory receptors and play a vital role in eliciting airway reflexes is considerably new (29). This concept is indirectly supported from findings that vagally mediated airway reflexes evoked by inhaled cigarette smoke (27), inhaled wood smoke (22), or pulmonary air embolism (6) and responses of vagal sensory receptors to the latter two insults (7,24,25) are greatly attenuated b...

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Section: Discussionmentioning

confidence: 99%

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

Ruan

Kou

2003

Journal of Applied Physiology

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“…For example, oxidative activation of the transient receptor protein A1 (TRPA1) of the pulmonary epithelium by hydrogen peroxide was investigated in mice and its activation by diamide was investigated in perfused guinea pig lung (Bannenberg et al 1994;Bessac et al 2008). …”

Section: Mak Value Documentations 1038mentioning

confidence: 99%

Azodicarbonamide [MAK Value Documentation, 2017]

Hartwig

Arand²

2018

The MAK‐Collection for Occupational Health and Safety

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The German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area has evaluated azodicarbonamide [123‐77‐3] to derive a maximum concentration at the workplace (MAK value), considering all toxicological endpoints. Available publications and unpublished study reports are described in detail. The critical effect is the occurrence of reactions in the airways in exposed workers. In the view of the Commission, the present inhalation studies in animals are not appropriate for the derivation of a MAK value as human airways are probably more sensitive than rodent airways. The workplace investigations show no clear correlation of exposure and frequency of respiratory symptoms. Nevertheless, from the NOAEC of 36 µg/m 3 for lung function measurements in a small group of injection‐molding workers in the plastics industry, a MAK value of 20 µg/m 3 I is established. Due to the incomplete information on the relevant exposure scenario and the uncertainty regarding first occurrence of workplace related symptoms, this value should be considered as preliminary. As local effects are critical, azodicarbonamide is assigned to Peak Limitation Category I and the default excursion factor of 1 is designated. Since developmental toxicity studies are not available, Pregnancy Risk Group D is assigned. There are no carcinogenicity studies and azodicarbonamide is not regarded as germ cell mutagen. Skin contact is not expected to contribute significantly to systemic toxicity. The metabolism of azodicarbonamide and its reactivity do not point to stable protein binding in vivo and therefore, skin or respiratory sensitization is unlikely. Clear‐cut clinical findings or positive results from animal studies on skin sensitization are not available, but the negative results in experimental animals are difficult to evaluate due to the low solubility of the compound. Although azodicarbonamide affects the respiratory tract in several case reports with positive bronchial provocation tests, sensitization by a known mechanism is not adequately verified. Additionally, it appears questionable whether a mono‐causal relationship of respiratory symptoms and azodicarbonamide exposure can really be assumed. In conclusion, a sensitizing effect of azodicarbonamide is not sufficiently proven. Completed: March 22, 2017

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Sensory neuropeptide-mediated bronchoconstriction of the guinea pig lung by diamide; a comparison to hydrogen peroxide

Cited by 2 publications

References 40 publications

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

Azodicarbonamide [MAK Value Documentation, 2017]

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