Therapeutic doses of ephedrine produce mainly relaxation of smooth muscle and, if norepinephrine stores are intact, cardiac stimulation and increased systolic and usually increased diastolic blood pressure. Its vasopressor effect results largely from increased cardiac output and to a lesser extent from peripheral vasoconstriction. Pressor responses to parenteral ephedrine are slower but more prolonged than those produced by epinephrine. Ephedrine stimulates both alpha and beta receptors and its peripheral actions are due partly to norepinephrine release and partly to direct effect on receptors. Ephedrine may deplete norepinephrine stores in sympathetic nerve endings, so that tachyphylaxis to cardiac and pressor effects of the drug may develop. Central nervous system effects are similar to those of amphetamine drugs but less pronounced. The central effects of ephedrine are overshadowed to a large extent by its peripheral actions. Glycogenolysis in the liver is increased by ephedrine but not as much as by epinephrine; usual doses of ephedrine are unlikely to produce hyperglycemia. Ephedrine increases oxygen consumption and metabolic rate as a probable result of central stimulation.

Ephedrine is rapidly and completely absorbed following parenteral injection. Pressor and cardiac responses to ephedrine persist for one hour following intramuscular or subcutaneous administration of 25 to 50 mg.

Small amounts of ephedrine are slowly metabolized in the liver; metabolites have been identified as p-hydroxyephedrine, p-hydroxynorephedrine, norephedrine, and conjugates of these compounds. The drug and its metabolites are excreted in the urine, mostly as unchanged ephedrine. Rate of urinary excretion is dependent on urinary pH. Percentage excretion of the drug and its metabolites is increased by acidification of the urine. Elimination half-life of the drug has been reported to be about three hours when the urine is acidified to pH 5 and about six hours when urinary pH is 6.3.

Bookmark this page: