Ergot (ergota) is a fungus which replaces the grain of rye. It rapidly deteriorates and should not be more than one year old. Our supply comes from Europe.


Though a vast amount of study was given to ergot for many years, its chemistry remained in a state of great confusion until Dale and his associates published their admirable studies in 1909 and 1910. We now recognize three very active alkaloids, ergotoxine, beta-iminazolylethylamine, and para-hydroxy-phenylethylamine, and two others, ergotine and isoamylamine. In addition there may be choline, and there are ergotinic acid, various saponins, and 20 to 35 per cent. of fat. A rare constituent, but one with a powerful depressant action on the circulation, is acetylcholine.

Ergotoxine is a hydrated ergotine. It is almost insoluble in water, but is soluble in alcohol. Its phosphate, which is soluble in water, is employed.

Para-hydroxy-phenylethylamine (tyramine), readily soluble in water, is closely related to certain amines found in unpurified cod-liver oil as the result of the putrefaction of the cod-livers.

It also bears a somewhat close chemical relation to epinephrine. It may be formed by the prolonged trypsin digestion of egg-albumin (Langestein, 1902), and was obtained by the action of a culture of human feces on broth to which tyrosin was added (Barger and Walpole, 1909); hence it is probably a product of intestinal putrefaction in some human cases. It has also been prepared synthetically.

Preparations And Doses

Ergot, 30 grains (2 gm.). Fluidextract (acetic), 30 minims (2 c.c.). Extract, 4 grains (0.25 gm.)

The alkaloids also may be employed - ergotoxine phosphate in dose of 1/50 grain (0.0012 gm.), and tyramine in dose of 1/2 grain (0.03 gm.) hypodermatically. They are not irritant. A very efficient artificial mixture containing the three important alkaloids in proper proportions to give a pronounced ergot action is to be had.


Up to the present no chemic assay has proved satisfactory. For the biologic assay three chief methods have been employed, viz., the blood-pressure method, which estimates the para-hydroxy-phenylethylamine, the uterine method which estimates the beta-iminazolylethylamine, and the cockscomb method, which estimates the ergotine. The first is not good, the pressor effect giving no indication of the contractile power of the drug upon the uterus. The uterine method is satisfactory, but is expensive and tedious. Edmunds and Hale and a number of others recommend the cockscomb method, finding it in very close agreement with the uterine method and much simpler. It is based on the development of a purple hue in the comb of a rooster from an injection of ergot. The standard is considered to be 0.75 c.c. of fluidextract per kilo, equivalent to 1.87 mg. of ergotoxine phosphate.


Ergot rapidly deteriorates unless kept from the air, and a number of investigators report that ergot and ergot preparations are useless if more than a year old. Yet this is not found to be the case in clinical experience, which corresponds more nearly with the experimental work of Haskell and Eckler (1912). They tested separately, and then mixed together, a large number of fluidextracts made in the different years. Those one and two years old gave a reaction in the standard amount, i. e., 0.75 c.c. per kilo. Those three years old required 1 c.c. for the reaction, and those four years old 1.5 c.c., and those five years old 1.75 c.c.

Pharmacologic Action

The active principles of ergot stimulate the ends of certain sympathetic nerves or their myoneural junctions. In large amounts ergotoxine paralyzes the same endings.


Ergot is irritant to mucous membranes and raw tissues. It has practically no constricting action on mucous membranes, but when injected hypo-dermatically produces a moderate constriction of the arteries at the point of injection. In some cases it has caused local gangrene.

Alimentary Tract

Preparations of ergot are irritant locally and may cause nausea, or, in poisoning, a violent gastroenteritis. The alkaloids are not irritant. The therapeutic doses of ergot stimulate the ends of the splanchnic (inhibitory) nerves, and cause decreased intestinal peristalsis. Very large doses cause paralysis of the same sympathetic nerve-endings, and result in increased peristalsis and activity of the bowels. This effect is not obtainable in therapeutics. In testing roosters it is usual for their bowels to move.


(A) Ergotoxine

Injected intravenously in a dog in dose of 1/65 grain (1 mg.) per kilo there is a prompt rise in arterial pressure with considerable slowing and weakening of the heart. A second injection makes a smaller rise in pressure or no change. An injection of epinephrine at this time causes dilatation of the arteries, the so-called "vasomotor reversal" of Dale. The ergotoxine at first stimulates and then paralyzes the myoneural junctions of the vasoconstrictor nerves, but leaves the vasodilator nerves untouched.

(b) Para-hydroxyphenylethylamine (ty-ramine) intravenously results in a prompt and marked rise in arterial pressure. This effect differs from that of epinephrine in its slower development, its four or five times as great duration, and its production (at least this is a claim put forward) by mouth and subcutaneous doses. The constriction of the arteries at the site of a hypodermatic injection is less than that from epinephrine, but it lasts longer and may result in local gangrene. Tests on human arterial pressure have been made by several observers. In a patient of Hoyt's with myocarditis, 40 mg. subcutaneously produced a rise of pressure from 85 to 130 mm. in five minutes, and the pressure had returned to its former level in nineteen minutes. By mouth Hoyt found that doses of 5 and 10 mg. three times a day, and Clark that a dose of 100 mg. repeated in forty minutes, had no effect.

Fig. 67.

Fig. 67. - Ergotized rye (Maisch).

(c) Beta-iminazolylethylamine intravenously in dose of 1/650 grain (0.1 mg.) per kilo produces an immediate and prolonged fall in blood-pressure due to an as yet unexplained peripheral action. It occurs after destruction of the central nervous system, but perfusion of isolated arteries results in contraction. The heart is slowed, but its output per minute is increased.

(D) The Whole Drug

Though the action of the active principles is, therefore, well known, the effect of preparations of ergot itself upon the circulation is problematic. For, given intravenously, ergot may induce a fall in pressure, as Sollmann and Brown (1905) found in 350 experiments on 38 animals; or it may cause a striking rise in pressure. The fall in pressure may be due to beta-iminazolylethylamine, to acetylcholine, or to the saponin bodies. In therapeutics, it is hardly possible to give enough ergot to obtain a rise in pressure, but a hypodermatic or intravenous of tyramine is a practical method of raising the arterial tension in emergency.