Involvement of hydroxyl radical in the immediate ventilatory responses to inhaled wood smoke in rats

Kou, Yu Ru; Lai, Chiung Ru; Hsu, Tien Huan; Lin, Yun‐Sheng

doi:10.1016/s0034-5687(96)02507-8

Cited by 20 publications

(31 citation statements)

References 18 publications

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“…In that pilot study, the doses of the latter two drugs were found to attenuate the H 2O2-evoked airway reflexes, and doubling the doses did not improve their suppressive effects on these airway reflexes. The doses of DMTU and Def were within the range reported previously in studies of ⅐ OH-related respiratory responses (11,22).…”

Section: Methodssupporting

confidence: 71%

“…In this study, pretreatment with Cat totally abolished all airway reflexive responses to H 2 O 2 challenge, whereas pretreatment with HiCat failed to do so, suggesting that these reflexive responses are consequences resulting from specific actions of H 2 O 2 . However, the latency of ventilatory responses to inhalation of H 2 O 2 aerosol observed in this study was much longer than those (within 1 or 2 s) to inhalation of other chemical irritants, such as cigarette (27,28) and wood smoke (22,23), in the same rat model; the effects of these two types of smoke are thought to be mediated through an oxygen radical mechanism. The long latency caused us to doubt whether lung C fibers and RARs are chemically stimulated by H 2 O 2 itself.…”

Section: Discussioncontrasting

confidence: 47%

“…Several studies have shown that ⅐ OH is the key reactive oxygen species involved in the stimulation of abdominal sympathetic afferents, cardiac sympathetic afferents, and cardiac vagal afferents by H 2 O 2 (18,40,44,48). Our laboratory previously reported that ⅐ OH scavengers attenuated airway reflexive responses or vagal afferent responses to inhaled wood smoke (22,24,25) or pulmonary air embolism (6, 7). These observations lead to the notion that reactive oxygen species may stimulate pulmonary sensory receptors and evoke airway reflexes.…”

Section: Discussionmentioning

confidence: 99%

“…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 by pretreatment with ⅐ OH scavengers. The evidence is not limited to sensory receptors located in the lower airways, because airway reflexes evoked by wood smoke-induced stimulation of nasal (17) and laryngeal (30) afferents are also inhibited by pretreatment with ⅐ OH scavengers.…”

mentioning

confidence: 88%

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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: Methodssupporting

confidence: 71%

Section: Discussioncontrasting

confidence: 47%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 88%

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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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“…Reactive oxygen species have been postulated as a factor mediating the inflammatory response in previous studies (19,20). Irritation caused by wood smoke leading to bradycardia has also been demonstrated as a result of hydroxyl radicals (16,21). In the present study, cumulative effects were not observed after 3 days of exposure.…”

Section: Discussionsupporting

confidence: 48%

Effects of concentrated ambient particles on heart rate and blood pressure in pulmonary hypertensive rats.

Cheng

Hwang

Wang

et al. 2003

Environ Health Perspect

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Epidemiologic studies have shown that increased concentrations of ambient particles are associated with cardiovascular morbidity and mortality (1,2). However, the mechanisms of such associations have not been clearly defined. Recent epidemiologic studies have found associations of increased air particles with increased heart rate and blood pressure and decreased heart rate variability (3-6). It has been speculated that particles cause the activation of autonomic nervous system, leading to changes in heart rates (7). To clarify the relationship of particles with mortality and morbidity, animal models have been used to investigate the effects of particles (8,9). Preliminary studies revealed increased heart rates and arrhythmia in pulmonary hypertensive rats after exposure to concentrated ambient particles (8,10,11). However, a recent study revealed a decreased heart rate when residual oil fly ash was instilled into the rats (12). To investigate further the mechanisms of particleinduced cardiotoxicity, we used heart rate and blood pressure as outcome indicators to assess their association with concentrated ambient particles in pulmonary hypertensive rats. Studies have also indicated that particles with aerodynamic diameter < 2.5 µm (PM 2.5 ) exert greater adverse health effects than coarse particles (1,13). To investigate the effects of PM 2.5 on cardiovascular diseases, we used an ambient particle concentrator, which generated PM 2.5 , to test our hypothesis (14).It is a common practice to divide experimental animals into exposure and control groups to study the effects of air particles. Because of the wide variation among diseased animals, this method requires large numbers of animals to delineate the true effect of air particles (9). Furthermore, variation in circadian cycle for individual rats also makes comparisons of heart rate or blood pressure difficult. To overcome this problem, we used each animal as its own control by exposing the individual animals repeatedly to concentrated air and filtered air and successfully detected the effects of particles on heart rate and mean blood pressure in three rats. Materials and MethodsAnimals and development of pulmonary hypertension. Male Sprague-Dawley rats 60 days old were obtained from the National Laboratory Animal Breeding and Research Center, housed in plastic cages on Aspen chip bedding, and provided with Lab Diet 5001(PMI Lab, Montville, NJ, USA) and water ad libitum except during exposure.Animals were maintained on a 12-hr light/ dark cycle at 22 ± 1°C and 55 ± 10 % relative humidity. We injected rats with monocrotaline intraperitoneally at 60 mg/kg body weight to cause them to develop pulmonary hypertension. Fourteen days after monocrotaline injection, animals were ready for experimentation (15).Experimental design. Ambient particles from the Chung-Li area, a suburb of Taipei, were concentrated through a modified ultrafine particle concentrator developed by Sioutas et al. (14). Briefly, the particle concentrator used virtual impactor technology in which 110 L...

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Thermally responsive poly[N‐isopropylacrylamide‐co‐2‐hydroxyethylacrylate] colloidal crystals included in β‐cyclodextrin for controlled drug delivery

Mathews¹,

Cho²,

Kim³

et al. 2009

J of Applied Polymer Sci

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Novel temperature-sensitive poly [N-isopropylacrylamide-co-2-hydroxyethylacrylate] [P(NIPAAmHEAc)] colloidal crystals containing b-cyclodextrin (b-CD) were prepared. These reversibly tunable supramolecular inclusion complexes display brilliant colors, due to the self-assembly of several structured nanoparticles to form crystal structures. The hydrogels displayed rainbow colors upon the variation of the b-CD concentration and can be made either visible or invisible by simply changing the temperature. The inclusion complexes were characterized using NMR spectroscopy, laser light scattering, UV-visible spectroscopy, and viscometer measurements. Compared with the conventional poly(N-isopropylacrylamide) gel, the b-CD-incorporated hydrogels in aqueous solution showed a lower critical solution temperature of about 57 C, which can be attributed to the hydrogen bonding between P(NIPAAm-HEAc) included in b-CD and water, which is enhanced by the hydrophilic groups of b-CD. The use of these materials as drug carriers was also evaluated by making use of their thermo-responsive behavior.The release time of a model drug, 5-fluorouracil (5-FU), from the novel inclusion complexes was prolonged in comparison to that from P(NIPAAm-HEAc) without b-CD. The significance of the present drug delivery system is the mixing of the gel and drug without any chemical reaction at room temperature, resulting in a gelled drug depot for slow and controlled release.

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Involvement of hydroxyl radical in the immediate ventilatory responses to inhaled wood smoke in rats

Cited by 20 publications

References 18 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

Effects of concentrated ambient particles on heart rate and blood pressure in pulmonary hypertensive rats.

Thermally responsive poly[N‐isopropylacrylamide‐co‐2‐hydroxyethylacrylate] colloidal crystals included in β‐cyclodextrin for controlled drug delivery

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