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The exemplary collaboration between engineering sciences and medicine has, in recent decades, developed electropacing of the heart into an extremely successful therapy. Due to high technological standards, cardiac pacemakers have become therapeutic agents that reliably reestablish cardiovascular function and improve the quality of life for a large number of patients. Their superiority over previous forms of treatment arises from the utilization of still existing physiological regulatory processes of the cardiovascular system. An understanding of natural impulse formation, impulse conduction, and replacement by artificial processes substantiates the success of the aforementioned interdisciplinary efforts.

The ingestion of food is necessary to cover the basic requirements of the body. The foodstuffs must not only cover the daily energy expenditure but also provide the substrates necessary for the functioning, structural maintenance and growth of the tissues and organs. The gastrointestinal (GI) tract processes the complex foodstuffs in order that nutrients may pass the intestinal wall and be transported in the blood to all parts of the body.

In recent clinical and experimental studies, vagotomy has given favorable results for peptic ulcers by reducing acid production through elimination of vagal stimuli [1]. Experimental gastric ulceration and bleeding caused by immobilization stress or a stereotactic hypothalamic lesion, however, can be prevented by vagotomy or sympathectomy [2].

Previous studies have shown that automaticity and conduction in various cardiac tissues can be accelerated, decelerated, or suppressed completely (annihilated) by properly timed short bursts of vagal discharges [1, 12–15, 18, 23, 26, 28–30, 33]. Phase-resetting and annihilation of automaticity and conduction also can occur following the delivery of brief hyperpolarizing or depolarizing current pulses [3, 7–11]. These observations suggest that cardiac arrhythmias caused by automaticity or by conduction abnormalities may be modulated by phasic discharges of the autonomic nervous system.

It has been known for over a century that the cardiac glycosides affect the autonomic nervous system and that both the sympathetic and parasympathetic components can be involved. This review will look mainly at the evidence for the autonomic effects of peripherally administered cardiac glycosides as well as postulated mechanisms and will not consider in great detail work concerned with the effects of the cardiac glycosides on the central nervous system.

Our purpose in this chapter is to review the cellular electrophysiologic effects of autonomic stimulation, and to demonstrate its complexity in two ways: by describing the changes in cardiac autonomic interactions that occur with growth and development, and by describing how autonomic mediators modulate cardiac arrhythmias.

The esophagus may be regarded as a tube extending from pharynx to stomach and serving for transport of material between these two organs. At rest (i.e., between swallows and regurgitations), sphincter mechanisms at either end of the tube prevent easy access of air from above and gastric contents from below. For purposes of clarity the control of the tubular esophagus (or esophageal body) and that of the sphincter areas will be dealt with separately.

Among all vagal stimulation tests in clinical use the insulin test is the most important, while the D-d-G-test is of higher risk and sham-feeding in humans has no good reproducible results. By Insulin-test the cephalic phase of gastric secretion can be examined. The insulin test is suitable for checking the completeness of vagotomy because it shows the degree of reduction of vagally stimulated acid secretion. So the effect on elimination of ulcerogenic interdigestive secretion can be evaluated. After SPV, in spite of complete removal of vagally stimulated acid secretion both after insulin stimulation in humans (Fig. 18) and after sham-feeding in dogs, a significant increase of vagally released gastrin was observed (Fig. 19) [16, 102 p. 83]. However, at least after insulin stimulation, there are some doubts that this release of gastrin is related only to vagal influences.

When the left lobe of the liver is retracted upward and the stomach pulled downward, the abdominal portion of the esophagus can be seen. In thin patients, in particular, the anterior vagus trunk (trunk diameter 0,3 to 6 mm) is visible, covered by its serous coat, anterior to the abdominal portion of the esophagus. The posterior vagus trunk (trunk diameter 0,2 to 7 mm) cannot be seen but can usually be palpated. If the esophagus is rotated around its longitudinal axis, the posterior vagus trunk can be seen. The opinion cited in many textbooks of anatomy and surgery, that there is only one anterior ( = left) vagus trunk and one posterior vagus ( = right) vagus trunk should be regarded skeptically. As in the description of Harkins (1962) Hrabal (1974) has stated that the following distribution of vagus trunks may be expected in the abdominal portion of the esophagus: $$ \begin{array}{l} anterior\,\,vagus\,\,trunk:\,\,{\rm{1}}\,\,{\rm{trunk}}\,{\rm{ - }}\,{\rm{27,6\% ,}}\,\,{\rm{2}}\,\,{\rm{trunks}}\,\,{\rm{ - }}\,{\rm{27,7\% ,}}\,\,{\rm{3}}\,\,{\rm{trunks}}\,{\rm{ - }}\,{\rm{20,7\% ,}}\,\,{\rm{4}}\,\,{\rm{trunks}}\\ {\rm{13,8\% , 5}}\,\,{\rm{trunks}}\,\,{\rm{ - }}\,\,{\rm{8,5\% ,}}\,\,{\rm{and}}\,\,{\rm{6}}\,{\rm{trunks}}\,\,{\rm{ - }}\,{\rm{1,7\% ;}} \end{array} $$ $$ \begin{array}{l} posterior\,vagus\,\,trunk:\,\,{\rm{1}}\,\,{\rm{trunk}}\,\,{\rm{ - }}\,\,{\rm{40\% ,}}\,\,{\rm{2}}\,\,{\rm{trunks}}\,\,{\rm{ - }}\,\,{\rm{28,4\% ,}}\,\,{\rm{3}}\,\,{\rm{trunks}}\,\,{\rm{ - }}\,\,{\rm{18,4\% ,}}\,\,{\rm{4}}\,\,{\rm{trunks}}\\ {\rm{10\% ,}}\,{\rm{6}}\,\,{\rm{or}}\,\,{\rm{7}}\,\,{\rm{trunks}}\,\,{\rm{ - }}\,\,{\rm{3,2\% }}\,\,{\rm{(Fig}}{\rm{.1)}}{\rm{.}} \end{array} $$