Eucapnic Hyperventilation-Induced Bronchoconstriction in Rabbits.

Koyama, Shinichiro; Ohtsuka, Akiko; Horie, Takashi

doi:10.1620/tjem.168.611

Cited by 5 publications

(6 citation statements)

References 28 publications

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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: 72%

“…In guinea-pigs [14], rabbits [8], and dogs [58] AIB does not usually develop until after hyperpnoea stops. In man, it can occur during exercise [127], but is more common when exercise stops [23].…”

Section: The Acute Responsementioning

confidence: 99%

“…Studies of allergic rabbits also implicate a role for histamine in AIB (table 1). However, chlorpheniramine was used to inhibit H 1 -receptors in the rabbit [8], and this drug can also inhibit vagal activity [147]. In contrast, AIB in guinea-pigs appears to be independent of histamine (table 1).…”

Section: Calcium Antagonistsmentioning

confidence: 99%

“…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]). c) Dogs: hyperventilated with 2,000 mL·min -1 for 5 min ( ---❍ ---) (data from FREED and ADKINSON [9]); hyperventilated with 1,500 mL·min -1 for 2 min ( ∆ ) (data from FREED and co-workers [10]).…”

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confidence: 99%

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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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Section: Calcium Antagonistsmentioning

confidence: 72%

Section: The Acute Responsementioning

confidence: 99%

Section: Calcium Antagonistsmentioning

confidence: 99%

mentioning

confidence: 99%

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Models and mechanisms of exercise-induced asthma

An¹

1995

Eur Respir J

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“…2) Scavengers of hydroxyl radicals (dimethylthiourea) [28] as well as the combination of superoxide dismutase and catalase, significantly suppressed the HIB induced by hyperpnoea with a high O 2 gas mixture [3]. 3) HIB was found to occur more frequently in sensitized rabbits [29]. It is known that there is an increase in oxygen radical production in sensitized animals [30].…”

Section: Chronic Hypoxia Antioxidants and Hyperpnoea-induced Bronchomentioning

confidence: 98%

Attenuation of isocapnic hyperpnoea-induced guinea-pig bronchoconstriction by chronic hypoxia

Lai¹,

Lin²,

Lai³

1998

Eur Respir J

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Decreases in both water vapour and temperature in airways occur during hyperpnoea. Hyperpnoea-induced bronchoconstriction (HIB) is caused by water or heat loss, or both, immediately following hyperpnoea. RAY et al. [1] demonstrated that HIB is mediated by tachykinins in guineapigs. Similarly, SOLWAY et al. [2] blocked HIB in guineapigs by using tachykinin receptor antagonists, especially the neurokinin-2 receptor antagonist. However, the relationship between the magnitude of HIB and tachykinin levels is not clear.It has been demonstrated previously that oxygen radicals play an important role in HIB [3,4]. In these studies, oxygen radical scavengers and antioxidants significantly reduced tachykinin-mediated HIB. Oxygen radicals may augment HIB via an increase in tachykinin release and/or inactivation of neutral endopeptidase (NEP). NEP is the major degradation enzyme for tachykinins. Oxygen radicals may activate afferent C-fibres of the lungs and induce tachykinin release. This stimulation of afferent C-fibres has been demonstrated in visceral afferents [5]. It is also known that NEP is inactivated by oxygen radicals and is protected by antioxidants [6].FRANK [7] demonstrated that chronic hypoxia enhances the production of antioxidant enzymes in rat lungs. It is not clear whether the same phenomenon occurs in guineapig lungs. Antioxidants attenuate acute lung oedema induced by xanthine-xanthine oxidase (X-XO) [8], which is known to generate oxygen radicals [9]. Therefore, the bronchial response to X-XO was used to test indirectly the antioxidant defence levels in the lungs before and after chronic hypoxic exposure in guinea-pigs. Following the indirect evidence of increased antioxidant defence levels caused by chronic hypoxia, the question of whether HIB can be attenuated by pretreating guinea-pigs with chronic hypoxia was explored. Furthermore, both tachykinin level and NEP activity were investigated for the possible underlying effects of chronic hypoxia. Materials and methods Preparation of experimental animalsThirty young, male Hartley guinea-pigs (from the Animal Centre, National Science Council, Taipei, Taiwan) weighing 232±14 g were divided into four groups: control (n=8); chronic hypoxia (n=7); capsaicin pretreatment (n= 7); and capsaicin pretreatment plus chronic hypoxia (n= 8). Animals in the control group were placed in an opened hypobaric chamber with no subatmospheric pressure. Animals in the chronic hypoxia group were placed in the closed hypobaric chamber with a barometric pressure of 380 mmHg [10] for 7 days. The animals were only Attenuation of isocapnic hyperpnoea-induced guinea-pig bronchoconstriction by chronic hypoxia. Y-L. Lai, C.W. Lin, L-C. Lai. ©ERS Journals Ltd 1998.ABSTRACT: Chronic hypoxia has been shown to augment the production of antioxidants in rat lungs and to reduce airway hyperreactivity in patients with asthma. This study investigated indirectly whether this increase in antioxidants occurs in guineapig lungs and whether the increased antioxidants affect hyperpnoea-induced bro...

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Pulmonary Smooth Muscle in Vertebrates: A Comparative Review of Structure and Function

Cieri

2019

Integrative and Comparative Biology

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Although the airways of vertebrates are diverse in shape, complexity, and function, they all contain visceral smooth muscle. The morphology, function, and innervation of this tissue in airways is reviewed in actinopterygians, lungfish, amphibians, non-avian reptiles, birds, and mammals. Smooth muscle was likely involved in tension regulation ancestrally, and may serve to assist lung emptying in fishes and aquatic amphibians, as well as maintain internal lung structure. In certain non-avian reptiles and anurans antagonistic smooth muscle fibers may contribute to intrapulmonary gas mixing. In mammals and birds, smooth muscle regulates airway caliber, and may be important in controlling the distribution of ventilation at rest and exercise, or during thermoregulatory and vocal hyperventilation. Airway smooth muscle is controlled by the autonomic nervous system: cranial cholinergic innervation generally causes excitation, cranial non-adrenergic, non-cholinergic innervation causes inhibition, and spinal adrenergic (SA) input causes species-specific, often heterogeneous contractions and relaxations.

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Eucapnic Hyperventilation-Induced Bronchoconstriction in Rabbits.

Cited by 5 publications

References 28 publications

Models and mechanisms of exercise-induced asthma

Models and mechanisms of exercise-induced asthma

Attenuation of isocapnic hyperpnoea-induced guinea-pig bronchoconstriction by chronic hypoxia

Pulmonary Smooth Muscle in Vertebrates: A Comparative Review of Structure and Function

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