ovalbumin and Hyperventilation

This study was carried out to determine the effect of allergic inflammation on the airway response to increasing airway temperature. Our results showed the following: 1) In Brown-Norway rats actively sensitized by ovalbumin (Ova), isocapnic hyperventilation with humidified warm air (HWA) for 2 min raised tracheal temperature (Ttr) from 33.4 ± 0.6°C to 40.6 ± 0.1°C, which induced an immediate and sustained (>10 min) increase in total pulmonary resistance (Rl) from 0.128 ± 0.004 to 0.212 ± 0.013 cmH2O·ml(-1)·s (n = 6, P < 0.01). In sharp contrast, the HWA challenge caused the same increase in Ttr but did not generate any increase in Rl in control rats. 2) The increase in Rl in sensitized rats was reproducible when the same HWA challenge was repeated 60-90 min later. 3) This bronchoconstrictive effect was temperature dependent: a slightly smaller increase in peak Ttr (39.6 ± 0.2°C) generated a significant but smaller increase in Rl in sensitized rats. 4) The HWA-induced bronchoconstriction was not generated by the humidity delivered by the HWA challenge alone, because the same water content delivered by saline aerosol at room temperature had no effect. 5) The HWA-evoked increase in Rl in sensitized rats was not blocked by atropine but was completely prevented by pretreatment either with a combination of neurokinin (NK)-1 and NK-2 antagonists or with formoterol, a β2 agonist, before the HWA challenge. This study showed that increasing airway temperature evoked a pronounced and reversible increase in airway resistance in sensitized rats and that tachykinins released from the vagal bronchopulmonary C-fiber endings were primarily responsible.

Topics: 2,4-Dichlorophenoxyacetic Acid; Aerosols; Airway Resistance; Animals; Atropine; Body Temperature; Bronchoconstriction; Humidity; Hypersensitivity; Hyperventilation; Inflammation; Male; Ovalbumin; Rats; Rats, Inbred BN; Tachykinins; Trachea; Vagus Nerve

Hyperventilation can induce bronchoconstriction in ovalbumin-sensitized rabbits. To investigate the roles of the beta-receptor parasympathetic nervous system and of chemical mediators in hyperventilation-induced bronchoconstriction (HIB), the effects of a beta 2-agonist, of sodium cromoglycate, and of an anticholinergic agent on HIB were studied. Rabbits were divided to four groups and treated as follows. Group 1: Control (n = 7, 0.9% saline); Group 2: Procaterol (n = 4, 50 micrograms/l); Group 3: Sodium cromoglycate (n = 4, 10 mg/ml); and Group 4: Ipratropium bromide (n = 6, 1 mg/ml). Each drug was inhaled for 1 min via an ultrasonic nebulizer. Then, for the eucapnic hyperventilation challenge, sensitized rabbits were mechanically hyperventilated for 15 min (120 breaths/min, tidal volume = 7 ml/kg) with dry air containing 5% CO2 at room temperature. Total lung resistance and dynamic compliance were measured before, and 0, 5, 15, and 30 min after hyperventilation. The mean percent change in resistance measured 5 min after the hyperventilation was +49% in group 1, -6% in group 2, +23% in group 3, and +1% in group 4. The changes in groups 2 and 4 were significantly less than in group 1 (p < 0.05). In conclusion, HIB is mainly caused by bronchial smooth muscle constriction, and chemical mediators and the parasympathetic nervous system may play important roles in the development of HIB in sensitized rabbits.

Topics: Acetylcholine; Adrenergic beta-Agonists; Animals; Bronchoconstriction; Cholinergic Antagonists; Cromolyn Sodium; Hyperventilation; Ipratropium; Ovalbumin; Procaterol; Rabbits; Vagus Nerve

We have demonstrated that hyperventilation-induced bronchoconstriction (HIB) is observed in sensitized rabbits, and that histamine may play a role in HIB. To investigate the role of parasympathetic neurotransmission in HIB, the effects of atropine and vagotomy on HIB were examined. Japanese white rabbits were sensitized with ovalbumin. They were then anesthetized and paralyzed with pancuronium, and then mechanically ventilated (TV: 7 ml/kg, RR: 40/min). The rabbits were divided into the following three groups: I) control group (n = 7), II) atropine-treated group (n = 6), III) bilateral vagotomy group (n = 6). Hyperventilation was performed at TV: 7 ml/kg, RR: 120/min for 15 min in dry room air containing 5% CO2. Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before and at 0, 5, 15 and 30 minutes after hyperventilation. RL increases significantly at 5 minutes in group 1, but this change was significantly less marked in groups 2 and 3. However Cdyn was not significant change in each group. We conclude that parasympathetic neurotransmission may play an important role in HIB of sensitized rabbits.

Topics: Animals; Atropine; Bronchoconstriction; Histamine; Hyperventilation; Ovalbumin; Parasympathetic Nervous System; Rabbits; Synaptic Transmission; Vagotomy

We examined whether eucapnic hyperventilation with dry air produces the bronchoconstriction in anesthetized, non-sensitized rabbits and in ovalbumin sensitized rabbits. Eucapnic hyperventilation challenge with dry air containing 5% CO2 at room temperature was performed with 4 non-sensitized and 7 sensitized rabbits by mechanical ventilation for 15 min (120 breaths/min, 7 ml tidal volume/kg body weight). Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before and 0, 5, 15, and 30 min after hyperventilation. In non-sensitized rabbits, RL and Cdyn did not change significantly. However, in sensitized rabbits, RL increased maximally by 48.9% +/- 9.0% at 5 min, and then decreased to the baseline level at 30 min after challenge. Cdyn decreased maximally by 12.5% +/- 3.5% at 15 min after challenge. These changes were significantly different from the baselines (p < 0.05). Furthermore, to investigate the role of histamine on hyperventilation-induced bronchoconstriction (HIB) in sensitized rabbits, we performed the hyperventilation challenges in 5 sensitized rabbits with the pretreatment of H1-receptor antagonist (chlorpheniramine, 1 mg/kg, i.v.) and found that the maximum increment of RL was suppressed to 24.2% +/- 7.4% of the control, which was significantly lower than the maximal RL in nontreated sensitized rabbits (p < 0.05). We concluded that HIB occurs only in sensitized rabbits and that histamine may play an important role in the development of HIB in sensitized rabbits.

Topics: Airway Resistance; Animals; Bronchoconstriction; Carbon Dioxide; Chlorpheniramine; Histamine; Hypersensitivity; Hyperventilation; Lung Compliance; Male; Ovalbumin; Physical Exertion; Rabbits