Kubota K, Ito S, Ohta T, Nakazato Y, Ohga A
Department of Pharmacology, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
Jpn J Vet Res. 1994 Dec;42(3-4):109-17.
The purpose of the present experiments was to examine the mechanism of the proventricular dilatation caused by lead in the isolated vagus nerve-proventricular smooth muscle preparation of the chick. Lead caused dose- and time-dependent inhibition of contractions induced by vagal stimulation, transmural stimulation and externally applied acetylcholine (ACh). Vagally evoked contraction was much more sensitive to the inhibitory action of lead than the contractile response to ACh. The lower the frequency of transmural stimulation, or the lower the concentration of ACh was applied, the greater the inhibitory action of lead on the evoked smooth muscle contraction. The results suggest that proventricular impaction occurring in lead poisoning results from the pre- and post-synaptic inhibition of the vagus nerve-smooth muscle transmission.
本实验的目的是在雏鸡离体迷走神经-嗉囊平滑肌标本中研究铅导致嗉囊扩张的机制。铅对迷走神经刺激、透壁刺激及外源性乙酰胆碱（ACh）诱导的收缩产生剂量和时间依赖性抑制。迷走神经诱发的收缩比ACh引起的收缩反应对铅的抑制作用更敏感。透壁刺激频率越低，或施加的ACh浓度越低，铅对诱发的平滑肌收缩的抑制作用就越大。结果表明，铅中毒时发生的嗉囊阻塞是由于迷走神经-平滑肌传递的突触前和突触后抑制所致。
