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Bodily changes in pain, hunger, fear, and rage

Chapter 104: REFERENCES
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A systematic account of experiments examining physiological changes that accompany pain, hunger, fear, and rage. It explains autonomic nervous system organization and shows how emotional excitation alters digestion, circulation, respiration, coagulation, and glandular secretion. Experimental evidence links splanchnic nerve activity and adrenal secretion to rapid increases in blood pressure, mobilization of energy, inhibition of intestinal motility, and accelerated clotting; hunger sensations and gastric contractions are described alongside methods used to record them. The work argues that these coordinated visceral reactions are adaptive responses to threat or need and provides detailed experimental procedures and results supporting a functional interpretation of emotional bodily changes.

Figure 39.—One-half the original size. The top record represents compression of thin rubber bag in the lower esophagus. The pressure in the bag varied between 9 and 13 centimeters of water. The cylinder of the recorder was of smaller diameter than that used in the gastric records. The esophageal contractions compressed the bag so completely that, at the summits of the large oscillations, the respirations were not registered. When the oscillations dropped to the time line, the bag was about half inflated. The middle line registers time in minutes (ten minutes). The bottom record is W’s report of hunger pangs.

This study of hunger, reported by Washburn and myself in 1912, has since been taken up by Carlson of Chicago, and in observations on a man with a permanent gastric fistula, as well as on himself and his collaborators, he has fully confirmed our evidence as to the relation between contractions of the alimentary canal and the hunger sensation. In a series of nearly a score of interesting papers, Carlson and his students[38] have greatly amplified our knowledge of the physiology of the “empty” stomach. Not only are there the contractions observed by Washburn and myself, but at times these may fuse into a continuous cramp of the gastric muscle. The characteristic contractions, furthermore, continue after the vagus nerve supply to the stomach has been destroyed, and, therefore, are not dependent on the reception of impulses by way of the cranial autonomic fibres. Recently Luckhardt and Carlson have brought forward evidence that the blood of a fasting animal if injected into the vein of a normal animal is capable of inducing in the latter the condition of cramp or tetanus in the gastric muscle mentioned above—an effect which does not occur when the blood of a well-fed animal is injected. It seems possible that a substance exists in the blood which acts to excite the gastric hunger mechanism. But this point will require further investigation.

With these demonstrations that contractions are the immediate cause of hunger, most of the difficulties confronting other explanations are readily obviated. Thus the sudden onset of hunger and its peculiar periodicity—phenomena which no other explanation of hunger can account for—are at once explained.

In fever, when bodily material is being most rapidly used, hunger is absent. Its absence is understood from an observation made by F. T. Murphy and myself,[39] that infection, with systemic involvement, is accompanied by a total cessation of all movements of the alimentary canal. Boldireff observed that when his dogs were fatigued the rhythmic contractions failed to appear. Being “too tired to eat” is thereby given a rational explanation.

A pathological form of the sensation—the inordinate hunger (bulimia) of certain neurotics—is in accordance with the well-known disturbances of the tonic innervation of the alimentary canal in such individuals.

Since the lower end of the esophagus, as well as the stomach, contracts periodically in hunger, the reference of the sensation to the sternum by the ignorant persons questioned by Schiff was wholly natural. The activity of the lower esophagus also explains why, after the stomach has been removed, or in some cases when the stomach is distended with food, hunger can still be experienced. Conceivably the intestines also originate vague sensations by their contractions. Indeed, the final banishment of the modified hunger sensation in the patient with duodenal fistula, described by Busch, may have been due to the lessened activity of the intestines when chyme was injected into them.

The observations recorded in this paper have, as already noted, numerous points of similarity to Boldireff’s observations[40] on the periodic activity of the alimentary canal in fasting dogs. Each period of activity, he found, comprised not only widespread contractions of the digestive canal, but also the pouring out of bile, and of pancreatic and intestinal juices rich in ferments. Gastric juice was not secreted at these times; when it was secreted and reached the intestine, the periodic activity ceased. What is the significance of this extensive disturbance? I have elsewhere presented evidence[41] that gastric peristalsis is dependent on the stretching of gastric muscle when tonically contracted. The evidence that the stomach is in fact strongly contracted in hunger—i. e., in a state of high tonus—has been presented above.[*] Thus the very condition which causes hunger and leads to the taking of food is the condition, when the swallowed food stretches the shortened muscles, for immediate starting of gastric peristalsis. In this connection the observations of Haudek and Stigler[42] are probably significant. They found that the stomach discharges its contents more rapidly if food is eaten in hunger than if not so eaten. Hunger, in other words, is normally the signal that the stomach is contracted for action; the unpleasantness of hunger leads to eating; eating starts gastric digestion, and abolishes the sensation. Meanwhile the pancreatic and intestinal juices, as well as bile, have been prepared in the duodenum to receive the oncoming chyme. The periodic activity of the alimentary canal in fasting, therefore, is not solely the source of hunger pangs, but is at the same time an exhibition in the digestive organs of readiness for prompt attack on the food swallowed by the hungry animal.

* The “empty” stomach and esophagus contain gas (see Hertz: Quarterly Journal of Medicine, 1910, iii, p. 378; Mikulicz: Mittheilungen aus den Grenzgebieten der Medicin und Chirurgie, 1903, xii, p. 596). They would naturally manifest rhythmic contractions on shortening tonically on their content.

REFERENCES

1 Cannon: The Mechanical Factors of Digestion, London and New York, 1911, p. 204.

2 Bardier: Richet’s Dictionnaire de Physiologie, article Faim, 1904, vi, p. 1. See, also, Howell: Text-book of Physiology, fourth edition, Philadelphia and London, 1911, p. 285.

3 See Sternberg: Zentralblatt für Physiologie, 1909, xxii, p. 653. Similar views were expressed by Bayle in a thesis presented to the Faculty of Medicine in Paris in 1816.

4 See Hertz: The Sensibility of the Alimentary Canal, London, 1911, p. 38.

5 Schiff: Physiologie de la Digestion, Florence and Turin, 1867, p. 40.

6 Luciani: Das Hungern, Hamburg and Leipzig, 1890, p. 113.

7 Tigerstedt: Nagel’s Handbuch der Physiologie, Berlin, 1909, i, p. 376.

8 Johanson, Landergren, Sonden and Tigerstedt: Skandinavisches Archiv für Physiologie, 1897, vii, p. 33.

9 Carrington: Vitality, Fasting and Nutrition, New York, 1908, p. 555.

10 Viterbi, quoted by Bardier: Loc. cit., p. 7.

11 Busch: Archiv für pathologische Anatomie und Physiologie und für klinische Medicin, 1858, xiv, p. 147.

12 See Schiff: Loc. cit., p. 37; also Ducceschi; Archivio di Fisiologia, 1910, viii, p. 579.

13 Longet: Traité de Physiologie, Paris, 1868, i, p. 23.

14 Ludwig: Lehrbuch der Physiologie des Menschen, Leipzig and Heidelberg, 1858, ii, p. 584.

15 Maxwell: Journal of Biological Chemistry, 1906–7, ii, p. 194.

16 See Schiff: Loc. cit., p. 49.

17 See Schiff: Loc. cit., p. 31; Bardier; Loc. cit., p. 16.

18 Head: Brain, 1893, xvi, p. 1; 1901, xxiv, p. 345.

19 Nicolai: Ueber die Entstehung des Hungergefühls, Inaugural Dissertation, Berlin, 1892, p. 17.

20 Beaumont: The Physiology of Digestion, second edition, Burlington, 1847, p. 51.

21 Nicolai: Loc. cit., p. 15.

22 Beaumont: Loc. cit., p. 55.

23 Luciani: Archivio di Fisiologia, 1906, iii, p. 54. Tiedemann long ago suggested that gastric nerves become increasingly sensitive as fasting progresses. (Physiologie des Menschen, Darmstadt, 1836, iii, p. 22.)

24 Valenti: Archives Italiennes de Biologie, 1910, liii, p. 94.

25 Weber: Wagner’s Handwörterbuch der Physiologie, 1846, iii2, p. 580.

26 Vierordt: Grundriss der Physiologie, Tübingen, 1871, p. 433.

27 Schiff: Loc. cit., p. 33.

28 Luciani: Loc. cit., p. 542.

29 Valenti: Loc. cit., p. 95.

30 Bettmann: Philadelphia Monthly Medical Journal, 1899, i, p. 133.

31 Wolff: Dissertation, Giessen, 1902, p. 9.

32 His: Archiv für Anatomie, 1903, p. 345.

33 Boldireff: Loc. cit., p. 1.

34 Boldireff: Loc. cit., p. 96.

35 See Cannon and Lieb: American Journal of Physiology, 1911, xxix, p. 267.

36 Ducceschi: Archivio per le Scienze Mediche, 197, xxi, p. 154.

37 See Cannon: American Journal of Physiology, 1903, viii, p. xxi; 1905, xiv, p. 344.

38 See American Journal of Physiology, 1913, 1914.

39 Cannon and Murphy: Journal of the American Medical Association, 1907, xlix, p. 840.

40 Boldireff: Loc. cit., pp. 108–111.

41 Cannon: American Journal of Physiology, 1911, xxix, p. 250.

42 Haudek and Stigler: Archiv für die gesammte Physiologie, 1910, cxxxiii, p. 159.