Sjöqvist A, Brunsson I, Theodorson E, Brodin E, Jodal M, Lundgren O
Department of Physiology, University of Göteborg, Sweden.
Acta Physiol Scand. 1993 Aug;148(4):387-92. doi: 10.1111/j.1748-1716.1993.tb09574.x.
The possible involvement of tachykinins in the nervous reflex activated by exposing the intestinal mucosa to cholera toxin was investigated in cats and rats. Three types of experiments were performed. In cats the release of tachykinins into blood was followed after placing cholera toxin in the intestinal lumen. In rat experiments a tachykinin receptor antagonist (Spantide II) was given close i.a. and its effect on cholera toxin-evoked fluid secretion was studied. Finally, in rats the effect of cholera toxin on the SP contents in the intestinal mucosa was studied. No release of tachykinins could be demonstrated. Spantide II did not change the rate of cholera toxin induced secretion. The SP content in the intestinal mucosa was not influenced by placing the toxin in the intestinal lumen. Hence, no experimental evidence was obtained for the involvement of a tachykinin neuron in the intestinal secretory nervous reflex activated by cholera toxin. Based on observations reported in the literature the involvement of an acetylcholine/tachykinin neuron in the reflex is tentatively discussed.
在猫和大鼠中研究了速激肽在暴露于霍乱毒素的肠黏膜所激活的神经反射中的可能作用。进行了三种类型的实验。在猫中,将霍乱毒素置于肠腔后,追踪速激肽向血液中的释放情况。在大鼠实验中,将速激肽受体拮抗剂(Spantide II)经肠内给药,研究其对霍乱毒素诱发的液体分泌的影响。最后,在大鼠中研究了霍乱毒素对肠黏膜中P物质含量的影响。未证实有速激肽的释放。Spantide II未改变霍乱毒素诱导的分泌速率。将毒素置于肠腔并未影响肠黏膜中的P物质含量。因此,未获得实验证据表明速激肽神经元参与了由霍乱毒素激活的肠分泌性神经反射。基于文献报道的观察结果,初步讨论了乙酰胆碱/速激肽神经元在该反射中的作用。