This section is from the book "Materia Medica: Pharmacology: Therapeutics Prescription Writing For Students and Practitioners", by Walter A. Bastedo. Also available from Amazon: Materia Medica: Pharmacology: Therapeutics: Prescription Writing for Students and Practitioners.
After atropine, stimulation of the chorda tympani results in no secretion of saliva. This is not due to the paralysis of the center or ganglia, for stimulation of the nerve peripheral to the ganglia still produces no secretion. Stimulation of the sympathetic, however, continues to cause secretion and vasodilatation, hence there is no paralysis of the secreting cells themselves or of the vasodilating fibers. Therefore the paralyzed portion is the connection between the nerve and the secreting cell, i. e., the nerve-ending. There is some evidence that in large amounts atropine slightly depresses the secretory cells themselves.
In the mouth the saliva and mucous secretions are lessened, and the throat and mouth become dry, an effect which is often noticed from quite small doses. If marked, the patient cannot swallow, though he may be very thirsty. The stomach secretion is less affected, but is probably moderately diminished by very large doses. Riegel states that this is especially true of the acid portion of the gastric juice.
The intestinal secretions tend to be lessened.
The secretion of the pancreas, though under the influence of the vagus, is dependent on the presence in the blood of the chemic substance secretin, rather than on nerve impulses, so atropine has little if any direct effect upon the amount of its digestive elements. But through depression of the vagus endings it may lessen the watery portion of the secretion.
The bile production has been shown also to be due partly to a substance in the blood, probably secretin, and its production is little, if any, affected.
It was formerly believed that by cutting off certain nerve impulses which induce the change of glycogen to sugar, atropine promoted the storing of glycogen by the liver, therefore it was recommended by Rudisch (1909) in diabetes. Forchheimer (1911) says of it: "In a large number of cases glycosuria, and with it acetone bodies, have diminished or disappeared." But in the very careful studies of two diabetics by Mosenthal (1912) atropine sulphate in amounts which gave beginning poisonous symptoms, i. e., up to 7/100 grain (0.0045 gm) three times a day, showed absolutely no effect on the carbohydrate tolerance.
In the stomach, atropine tends to overcome spasmodic contraction of the pylorus, but only when given in large doses hypodermatically. Indeed, Ochsenius in Czerny's clinic found that in a child of one month it required 1/85 to 1/70 grain (0.75 to 0.9 mg.) of atropine a day to relax the pylorus.
In the intestines, atropine lessens but does not abolish the vagus power (the vagus is the motor nerve of the small intestine), so that the effects of drugs which act as cathartics by stimulation of the vagus, e. g., physostigmine, may be checked; while the peristalsis from cathartics which act by direct irritation of the intestinal wall, and not through the vagus nerves, is apparently not affected. This is because atropine does not affect the automatic motor ganglia of Auerbach's plexus. (See Fig. 2, page 120.) It tends, however, to check the so-called "tone-waves" without checking peristalsis; and when from overirritation or from vagus overactivity there is spasmodic contraction with colicky pains, or spastic constipation, atropine tends to overcome this. To understand this action we must understand the difference between normal peristalsis and intestinal colic.
In peristalsis a wave of contraction precedes the stimulating body in the intestine by about an inch, while the bowel relaxes below the stimulating body for a foot or two. That is to say, peristalsis is a coordinated, purposeful action involving both stimulation and inhibition. It is designed to propel the intestinal contents forward and bring them into contact with the intestinal juices. But if, instead of this coordinated wave of contraction and relaxation, there is a spasmodic contraction of the intestine about some offending body, even about an accumulation of gas, or preceding an obstruction that cannot be moved onward, there is intestinal colic or cramp; at the same time the contents are not propelled along, so there is constipation. In such a case atropine, by allaying the spasm, may permit normal peristalsis to be restored, and, as a consequence, cause a disappearance of both the cramp and the constipation. Irritant cathartics sometimes cause this kind of colic, i. e., they tend to gripe, and to these atropine or one of the extracts is frequently added as a corrective. The constipation and colic of peritoneal irritation, anemia, lead poisoning, or fecal impaction may be overcome by atropine, but if the obstruction is immovable, i. e., of surgical nature, atropine obviously has no value.
Fig. 48. - Longitudinal muscle of small intestine immersed in saline. Tone waves are set up. The addition of 0.1 mg. of physostigmine sulphate at A results in tetanic contraction (cramp), which is abolished by the addition at B of 1 mg. of atropine sulphate. The normal peristaltic waves are restored, but not the tone waves. (Tracing made by Dr. C. C. Lieb.)
Fig. 49. - Chart showing the effects of atropine on the heart-rate of a patient with vagus slowing from digitalis. The numbers at the side represent pulse beats, those at the top, minutes (James Mackenzie, in "Heart," vol. ii. No. 4, 1911).