Hyperventilation-Induced Bronchoconstriction in Guinea Pigs

Chapman, Richard W.; Danko, Gisela

doi:10.1159/000233883

Cited by 29 publications

(14 citation statements)

References 20 publications

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“…Hyperventilation with dry air increases airway resistance in guinea pigs (1), rabbits (2), cats (3), dogs (4), monkeys (5), and humans (6). Other studies reveal that it damages the bronchial mucosa (7,8), increases bronchial blood flow (9,10), and increases bronchovascular permeability (8, 1 1 ).…”

Section: Introductionmentioning

confidence: 99%

The effect of bronchial blood flow on hyperpnea-induced airway obstruction and injury.

Freed¹,

Omori²,

Schofield³

1995

J. Clin. Invest.

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IntroductionWe examined the effect of bronchial blood flow (BBF) on hyperpnea-induced airway obstruction (HIAO) in dogs. HIAO in in situ isolated pulmonary lobes with or without BBF was monitored via a bronchoscope. An intravascular tracer in conjunction with morphometric analysis was used to document the efficacy of our occlusion technique. We found that (a) Occlusion of the bronchial artery abolished bronchovascular leakage, but did not alter HIAO; (b) HIAO occurred in postmortem dogs, and was attenuated by cooling; (c) absence of BBF did not cause mucosal damage, although hyperpnea-induced injury was enhanced in airways lacking BBF; (d) BBF did not affect either goblet/ ciliated cell ratios or hyperpnea-induced goblet cell degranulation; (e) ligation of the bronchial artery and hyperpnea each caused mast cell degranulation, and these effects were additive; (f) hyperpnea-induced leukocyte infiltration was reduced in the absence of BBF; and (g) ligation of the bronchial artery and hyperpnea with dry air each increased airway vessel diameter, and these effects were additive. We conclude that either impairment or absence of BBF abolishes bronchovascular leakage and increases hyperpnea-induced mucosal injury, but fails to affect HIAO. Based on these results we speculate that bronchovascular leakage protects the bronchial mucosa from excessive losses of heat and water, and inhibits mucosal damage. (J. Clin. Invest. 1995.

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Section: Introductionmentioning

confidence: 99%

The effect of bronchial blood flow on hyperpnea-induced airway obstruction and injury.

Freed¹,

Omori²,

Schofield³

1995

J. Clin. Invest.

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“…The fact that NK-receptor antagonists do not abolish AIB in guinea-pigs [69] suggests that other mediators or mechanisms account for the residual component in this model. The magnitude of AIB (measured as an increase over baseline resistance) elicited from guinea-pigs hyperventilated with hyperoxic gas [6,15] tends to be markedly greater than that reported for either this species [7,52], or other species [8,9,12,13], hyperventilated with normoxic gas ( fig. 1).…”

Section: Calcium Antagonistsmentioning

confidence: 73%

“…Unless otherwise specified, all species were hyperventilated with either dry room air or 5% CO 2 and dry air. a) Guinea-pigs: hyperventilated with dry gas containing 95% O 2 ( ---❍ ---) (data from RAY et al [6]); hyperventilated with dry gas containing 21% O 2 ( ∆ ) (data from CHAPMAN and DANKO [7]). b) Rabbits: sensitized to ovalbumin ( ---❍ ---); nonsensitized ( ∆ ) (data from KOYAMA et al [8]).…”

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confidence: 99%

Models and mechanisms of exercise-induced asthma

An¹

1995

Eur Respir J

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M Mo od de el ls s a an nd d m me ec ch ha an ni is sm ms s o of f e ex xe er rc ci is se e--i in nd du uc ce ed d a as st th hm ma a A.N. FreedModels and mechanisms of exercise-induced asthma. A.N. Freed. ERS Journals Ltd 1995. ABSTRACT: Airflow-induced bronchoconstriction (AIB) in mammals can be broadly categorized as either vagal-dependent or vagal-independent. Among mammals, rabbits and cats belong to the former and guinea-pigs belong to the latter categories. Although insufficient data are available to classify monkeys, dogs and man appear to occupy the middle ground in which a small but significant parasympathetic component modulates airflow-induced bronchoconstriction. The fact that vagal activity can only partially account for airflow-induced bronchoconstriction in some asthmatic subjects suggests that vagal-dependent models may be of limited value in studying the human condition, but should prove valuable in elucidating the parasympathetic component of this mechanism. Although airflow-induced bronchoconstriction appears to be remarkably similar in guinea-pigs, dogs and humans, there are important differences concerning the potential role of specific mediators in producing airflow limitation. Concordant data from animal models and man suggest that: 1) airflow-induced bronchoconstriction is a basic mammalian response to airway desiccation; 2) airway drying stimulates and cooling inhibits this response; 3) hyperpnoea with dry air may damage the bronchial mucosa and contribute to this response; 4) biochemical mediators contribute to the development of this response; 5) vascular engorgement and airway oedema do not appear to be the primary effectors of this response, and in fact may antagonize it; 6) airway smooth muscle constriction is involved in the production of airflow-induced bronchoconstriction, and airway oedema may enhance its effect; and 7) airway and vascular responses to dehydration may protect against acute dry air-induced mucosal injury.Finally, although one must be cautious in extrapolating results from animals to humans, the similarities that do exist suggest that the investigation of airflow-induced bronchoconstriction in carefully selected animal models will continue to provide new insights concerning its development in humans.

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“…Hyperpnea of cold and/or dry air precipi tates bronchoconstriction in anesthetized guinea pigs [11][12][13][14][15], The bronchoconstrictor response probably involves endogenously re leased tachykinins because the bronchospasm is potentiated by treatment with NEP inhibi tors [6,7] and is attenuated by selective NK-1 and NK-2 receptor antagonists [8], Further more. hvpcrpnea-induced bronchospasm in guinea pigs is reduced in animals depleted of sensory neuropeptides with capsaicin treat ment [6].…”

Section: Discussionmentioning

confidence: 99%

“…RL and Coyn were mea sured immediately before the start o f the hyperventila tion period and again 10 min after the hyperventila tion was terminated. This time was selected because we have previously found that peak changes in Rj and CDyn occur within 10 min o f terminating hyperventila tion [11], Only one hyperventilation challenge was giv en to each animal.…”

Section: Bronchoconstriction Due To Hyperventilationmentioning

confidence: 99%

Sch 37224, an Experimental Antiallergy Compound, Inhibits the Neuropeptide Component of Hyperventilation- and Nicotine-Induced Bronchoconstriction in Guinea Pigs

Mauser¹,

Rasquinha²,

Hey³

et al. 1997

Pharmacology

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Sch 37224 is an experimental antiallergy coumpound that inhibits hyperventilation-induced bronchoconstriction (HIB) in guinea pigs and cold air bronchospasm in human asthmatics. HIB in guinea pigs may involve the release of tachykinins, such as neurokinin A (NKA) and substance P (SP), and the action of Sch 37224 in this model may relate to inhibition of these neuropeptides. We studied the effect of Sch 37224 on the neuropeptide component of HIB that was enhanced in guinea pigs treated with the neutral endopeptidase inhibitors, thiorphan and phosphoramidon. Pulmonary resistance (R_L) and dynamic lung compliance (C_oyn) were measured in anesthetized, mechanically ventilated guinea pigs. R_L and C_Dyn were measured at baseline (1 ml/l00 g tidal volume and 50 breaths/min) and after a 10-min period of hyperventilation (1 ml/l00 g, 150 breaths/min). Hyperventilation produced modest changes in R_L (+41 ± 12%) and C_oyn (–12 ± 3%) which were markedly enhanced by treatment with 3 mg/kg of either thiorphan or phosphoramidon (Rl + 269 ± 43% for thiorphan, + 292 ± 63% for phosphoramidon and C_oyn –65 ± 3% for thiorphan, -51 ± 13% for phosphoramidon). In the presence of thiorphan or phosphoramidon, the bronchospasm to hyperventilation was significantly reduced (>70%) with 5 mg/kg, p.o., of Sch 37224. In other studies, the peptidergic (conducted in the presence of ipratropium bromide and phosphoramidon) bronchoconstrictor response to intravenous nicotine (1 mg/kg) was also inhibited by Sch 37224 (0.3-10 mg/kg, p.o.). However, Sch 37224 (5 mg/kg, p.o.) had no effect on the bronchoconstrictor response to intravenous NKA. These results indicate that Sch 37224 inhibits the neuropeptide component of HIB and nicotine in guinea pigs and this effect appears to be mediated by the inhibition of the release of tachykinins from airway C fibers.

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Hyperventilation-Induced Bronchoconstriction in Guinea Pigs

Cited by 29 publications

References 20 publications

The effect of bronchial blood flow on hyperpnea-induced airway obstruction and injury.

The effect of bronchial blood flow on hyperpnea-induced airway obstruction and injury.

Models and mechanisms of exercise-induced asthma

Sch 37224, an Experimental Antiallergy Compound, Inhibits the Neuropeptide Component of Hyperventilation- and Nicotine-Induced Bronchoconstriction in Guinea Pigs

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