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[Effects of a beta 2-agonist, sodium cromoglycate, and an anticholinergic agent on hyperventilation-induced bronchoconstriction in sensitized rabbits].

作者信息

Suguro H, Koyama S, Ohtsuka A, Horie T

机构信息

First Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Nihon Kyobu Shikkan Gakkai Zasshi. 1995 Aug;33(8):856-61.

PMID:7474566
Abstract

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.

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