Kizawa Y, Takayanagi I
Can J Physiol Pharmacol. 1985 Nov;63(11):1471-3. doi: 10.1139/y85-241.
Monkey (crab-eating monkey) was used as an experimental animal in this study since the pharmacological properties of isolated monkey bronchial smooth muscle were reported to be qualitatively similar to human muscle. Nicotine (10(-5)-10(-3) M) induced a phasic contraction in the isolated monkey bronchial smooth muscle preparation. The contractile response to nicotine was abolished by hexamethonium and atropine and potentiated by physostigmine but not influenced by tetrodotoxin. These results suggest that the response to nicotine was mediated through the release of acetylcholine, and that the nicotine-induced response may be produced through a sodium action potential independent process. In addition, the mechanisms of action of nicotine on the bronchial preparation of crab-eating monkey were similar to those of nicotine on the rabbit bronchial preparation but not to those on the isolated guinea-pig bronchus.
在本研究中,选用食蟹猴作为实验动物,因为据报道,分离出的猴支气管平滑肌的药理特性在性质上与人的肌肉相似。尼古丁(10⁻⁵ - 10⁻³ M)在分离的猴支气管平滑肌标本中诱导了阶段性收缩。六甲铵和阿托品可消除对尼古丁的收缩反应,毒扁豆碱可增强该反应,但河豚毒素对其无影响。这些结果表明,对尼古丁的反应是通过乙酰胆碱的释放介导的,并且尼古丁诱导的反应可能是通过独立于钠动作电位的过程产生的。此外,尼古丁对食蟹猴支气管标本的作用机制与对兔支气管标本的作用机制相似,但与对分离的豚鼠支气管的作用机制不同。