Abstract
Dixon, 1 Dale 2 and Loewi 3 originally established acetylcholine as the humoral agent that produces motility of the gastro-intestinal tract. Later research, recently summarised by Cannon 4 and Dale 5 has shown that acetylcholine is liberated by stimulation not only of parasympathetic nerves and sympathetic ganglia, but probably even with stimulation of striated muscle. Fröhner 6 reported that eserine was commonly used to produce increased peristaltic activity of the gastro-intestinal tract in animals; and since the work of Hunt, 7 Fühner 8 and Simonart, 9 it has been known that eserine added to acetylcholine greatly fortifies the action of acetylcholine. Matthes 10 and Loewi and Engelhart 11 have added to our knowledge that eserine prevents the hydrolysis of acetylcholine by blood and tissues through inhibiting an esterase. In the light of this knowledge, the authors investigated the effect of eserine and acetylcholine on ileus following peritonitis (to be published). In this research it was found that in peritonitis acetylcholine given intramuscularly in small doses produced either no effect or a very small one, but it was always effective when given with eserine. The present research was undertaken to investigate whether or not the stimulation of salivary secretion would produce motility of the intestine through liberation of acetylcholine from the stimulated salivary glands. Babkin, Alley and Stavraky 12 have demonstrated that acetylcholine is liberated into the venous blood when the chorda tympani was stimulated.
Healthy dogs under light ether anesthesia were used. Both chordae tympani were prepared and stimulated with weak faradic currents from a Harvard inductorium. Balloons were placed in the stomach, ileum and upper part of the colon, and connected with water manometers. Blood pressure was recorded in the usual way.
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