Undem B J, Adams G K, Buckner C K
Johns Hopkins University School of Medicine, Good Samaritan Hospital, Baltimore, Maryland.
J Pharmacol Exp Ther. 1989 Apr;249(1):23-30.
These studies examined the ability of electrical field stimulation (EFS) to influence antigen-induced responses in the guinea pig isolated trachea and main-stem bronchi. Airways isolated from guinea pigs actively sensitized to ovalbumin were superfused and stimulated transmurally with square pulses of 1 msec duration at a frequency of 16 pulses per sec. In the trachea, EFS caused an atropine-sensitive contraction followed by a maintained relaxation. The relaxation consisted of adrenergic and nonadrenergic components. In the bronchus, EFS caused a maintained contraction. This contraction was due to a combination of cholinergic (atropine-sensitive) and noncholinergic (capsaicin-sensitive) mechanisms. Histamine could not be detected in superfusate samples during electrical stimulation alone of either the trachea or bronchus. EFS significantly inhibited ovalbumin-induced tracheal contractions by about 30% without altering ovalbumin-induced histamine or immunoreactive peptido-leukotriene release from the tissues. EFS had a similar inhibitory effect on the contraction induced by application of exogenous histamine (10(-5) M). The electrical stimulus-induced inhibition of the antigen-induced contraction was abolished by tetrodotoxin and propranolol and reduced by a combination of atropine, propranolol and phentolamine. Norepinephrine (5 x 10(-6) M) inhibited ovalbumin-induced histamine release by about 30% without altering the contraction. Carbamylcholine had no effect on ovalbumin-induced histamine release. In the guinea pig bronchus, EFS stimulation had no effect on either histamine release or contraction induced by ovalbumin. These results demonstrate that in the guinea pig trachea nerve stimulation can significantly antagonize antigen-induced contractions and suggest that this is due to a functional antagonism by adrenergic and nonadrenergic relaxant neurotransmitters at the level of the airway smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
这些研究检测了电场刺激（EFS）对豚鼠离体气管和主支气管中抗原诱导反应的影响能力。从对卵清蛋白主动致敏的豚鼠分离出的气道进行灌流，并以1毫秒持续时间的方波脉冲、每秒16次脉冲的频率进行跨壁刺激。在气管中，EFS引起阿托品敏感的收缩，随后是持续的舒张。该舒张由肾上腺素能和非肾上腺素能成分组成。在支气管中，EFS引起持续的收缩。这种收缩是胆碱能（阿托品敏感）和非胆碱能（辣椒素敏感）机制共同作用的结果。在单独对气管或支气管进行电刺激期间，灌流液样本中未检测到组胺。EFS显著抑制卵清蛋白诱导的气管收缩约30%，而不改变卵清蛋白诱导的组胺或免疫反应性肽白三烯从组织中的释放。EFS对外源性组胺（10⁻⁵ M）诱导的收缩有类似的抑制作用。电刺激诱导的对抗原诱导收缩的抑制作用被河豚毒素和普萘洛尔消除，并被阿托品、普萘洛尔和酚妥拉明的联合用药减弱。去甲肾上腺素（5×10⁻⁶ M）抑制卵清蛋白诱导的组胺释放约30%，而不改变收缩。卡巴胆碱对卵清蛋白诱导的组胺释放无影响。在豚鼠支气管中，EFS刺激对卵清蛋白诱导的组胺释放或收缩均无影响。这些结果表明，在豚鼠气管中，神经刺激可显著对抗抗原诱导的收缩，并提示这是由于气道平滑肌水平上肾上腺素能和非肾上腺素能舒张性神经递质的功能性拮抗作用所致。（摘要截选至250字）
