Before Absorption

On the ingestion of strong alcoholic liquors there is an immediate rise in arterial pressure, the rate of the beat being accelerated. But though the action lasts only a few moments, it is an invaluable one in mild functional forms of collapse (feelings of faintness, fainting, etc.). From experiments with unanesthetized animals, Brooks reports that while alcohol placed in the mouth gave a striking reflex rise of arterial pressure, which returned to normal in five or ten minutes and was followed by a slow fall in pressure, alcohol placed in the stomach through a gastric fistula gave no rise in pressure, even in strengths up to 50 and 60 per cent. It is probable, therefore, that the reflex comes from the mouth. Well diluted alcoholic liquors have no reflex effect.

After Absorption

The effect of alcohol upon the circulation after absorption has been the subject of much controversy. Until a few years ago alcohol was in almost universal use as a powerful heart stimulant; while in recent years the pendulum has swung in the other direction, and comparatively little alcohol is prescribed. It might be in order, therefore, to review the pharmacologic data bearing on this point, remembering that studies in animals anesthetized by ether or chloroform tend to be misleading, because of the similarity of the alcohol action to that of these anesthetics.

At the Massachusetts General Hospital, Richard Cabot made 1105 observations in 58 cases of typhoid fever, pneumonia, heart disease, cirrhosis of the liver, pulmonary and peritoneal tuberculosis, and other conditions, to determine the clinical effect on arterial pressure. For the first twenty-four hours he gave 1/2 22 ounce (15 c.c.) of whisky, well diluted, every four hours, and during the second twenty-four hours 1 ounce (30 c.c.) every four hours. Observations were taken at first at 1/2-hour intervals, then every two hours, and finally every four hours. In no case did either the maximum or minimum arterial pressure show any change that could be attributed to the alcohol. These are valuable data, but their importance must not be exaggerated, for, as we have learned under Digitalis, arterial pressure, owing to man's sensitive mechanisms for regulating it, cannot be taken as a measure of the improvement of the circulation brought about by a drug.

The laboratory data may be summed up as follows:

On The Heart

In perfusing the coronaries of a dog's isolated heart, Langendorff and Loeb, independently, found that an addition to the perfusion fluid of 1/100 to 3/10 of 1 per cent. of alcohol (Langendorff used 0.01 to 0.1 per cent.; Loeb used 0.13 to 0.3 per cent.) resulted in increased strength of systole and increased output of the heart. This was not marked, as it would be from strophanthin or epinephrine, but was enough to measure. If, however, more than 1 per cent. of alcohol was added to the perfusion fluid, there was muscular depression with dilatation of the heart and stoppage in diastole. Wood and Hoyt (1905), working with a reptile heart, and with a nutritive perfusion fluid to eliminate any nutritive effect of alcohol, obtained practically the same results. With strengths of 0.25 and 0.5 per cent., the output from the heart was persistently increased. With strengths of 0.5 to 1 per cent. there was a primary increase, followed in a few minutes by a distinct decrease in the output. With strengths of over 1 per cent. and sometimes with strengths of less than this the muscular activity decreased at once. On changing from an alcoholic to a non-alcoholic perfusion fluid, the effect ceased quite promptly, the muscle readily giving up its alcohol. There were no destructive changes in the heart muscle or permanent impairment of its tone.

On the other hand, C. C. Lieb (1917) perfused the hearts of rabbits and cats with Ringer's solution free from dextrose. The addition of alcohol to make concentrations of less than 1 in 50,000 did not affect the heart at all. Alcohol to make concentrations above 1 in 50,000 resulted, in every case but one, in a decrease in the excursion and in the total amount of work, and usually in a decreased rate. There was no evidence that the normal heart or the heart exhausted after prolonged perfusion was capable of utilizing alcohol.

In fatigue and debility experiments Locke and others have shown that 0.5 per cent of dextrose in the blood will resuscitate a partly exhausted heart; and, as we have seen, many experiments show that alcohol can to some extent replace dextrose as a nutrient. Therefore it may be assumed that when other food material is not available, alcohol can serve as a nutritive to cardiac muscle as well as to skeletal muscle.

Alcohol, then, in moderate quantities, acts slightly as a direct stimulant to the heart muscle, and also probably in debilitated persons as energy-supplying food for the heart. In nervous, restless, excited persons it may result in a secondary quieting of the heart through its narcotic effect.

The rate of the heart is quickened, at first because of the reflex effect from the mouth, later because of direct depression of the vagus center (Dodge and Benedict).