The fact that the gastric hunger contractions involve essentially the same motor mechanisms as the gastric digestion contractions suggests that the chemical control exerted by the blood is probably the same on both. Esserine and pilocarpin augment the hunger contractions, while morphine produces profound inhibition (Luckhardt). Pituitrin produces an initial augmentation; epinephrin, amyl nitrite, calcium chloride, etc., a temporary depression.
Substances that cause temporary augmentation of the gastero-intestinal movements can apparently be prepared from all the tissues of the body. Attempts have been made to show that there is a specific "motor hormone" for gastero-intestinal peristalsis in the wall of the digestive tract itself. With the exception of epinephrin it is probable that all the substances so far studied in the various tissue extracts are abnormal split products or artifacts not present in normal blood, and hence playing no rdle either in the normal hunger contractions or in the digestion peristalsis. Biedl was not able to demonstrate any favorable action of spermin or testicle extracts on metabolism, appetite, or hunger. The fact that a drug or a tissue extract when introduced hypodermically or intravenously initiates or augments the gastric hunger contractions does not imply that these drugs or extracts have the same effect on the sensation of hunger. The latter effect may be modified or abolished by other actions, peripheral and central, of these substances.
The work of Bayliss and Starling, Magnus, Cannon, and others seemed to show that the gastero-intestinal contractions are primarily local reflexes through the Auerbach's plexus or initiated by "automatic" nervous discharges from the ganglionic plexus. Kieth reports the presence in the Auerbach's plexus of "nodal" tissue similar to that in the heart, and he ascribes the main rdle in the genesis of the gastero-intestinal movements to this nodal tissue. The presence of nodal tissue in the Auerbach's plexus does not materially alter the problem of the causation of the gastero-intestinal movements.
The special difficulties in relating the hunger contractions of the stomach to chemical changes in the blood arc the periodicity of the rhythm and the abrupt cessation of the contraction periods. So far as we know today chemical changes or starvation changes in the blood are more continuous. Of course, we do not <Jeny the possibility of a periodic secretion into the blood of some specific substance or hormone having this effect on the stomach, but all the evidence so far at hand is against this possibility. The fact that after extirpation of the parathyroid gland there is a tendency to atonicity and motor paralysis of the gastero-intestinal tract, especially when the symptoms of tetany are severe, is no evidence that the parathyroid secretion is a motor stimulus to the stomach and intestines. The motor paralysis is probably due to secondary causes. The only conclusion that seems warranted by the facts at hand is that the gastric hunger mechanism is primarily automatic or independent of blood changes as well as of central nervous r influences; but in the normal individual chemical changes of the f blood as well as nervous impulses from the brain and spinal cord augment or decrease this primary automatism in a way to correlate ■ it with the needs of the organism.
This conclusion should not be regarded as a bar to further investigation of the chemical control of the hunger mechanism in health, and especially in disease. Such work is not only urgent, but is certain to yield important results. Recent experiments by Dr. Luckhardt seem to show that the gastric hunger contractions in dogs are augmented by inducing the condition of phlorhizin glycosuria. It is significant that all the conditions which have so far proved to increase the hunger contractions (diabetes mellitus, pancreatic diabetes, prolonged starvation, great physical exertion, extreme cold, phlorhizin glycosuria) have these two things in common: (1) acidosis of varying degrees, and (2) either inability to use sugar by the tissues or else a lessened amount of sugar available for the use of the tissues because of the sugar having been oxidized or eliminated.