Motherwort
Botanical Description & Habitat
Leonurus cardiaca
Family
Labiatae
Common names
| Lion's ear | Lion's tail |
| Roman motherwort | Throw-wart |
Habitat
A native of central Asia and the United States. It is a perennial plant which grows in waste places and along roadsides, fences, and paths.
Description
Motherwort has an erect, stout stem, finely pubescent with a red-purple hue. It grows from two to three feet in height. The leaves are ovate, long, petioled, grow in opposite pairs, and are deeply divided, with three to seven lobes; they have a dark upper surface and a lighter underside. The flowers range from reddish-purple to white, grow in whorls from the leaf axils, and bloom from June to September.
Medicinal parts
Flowering tops and leaves
Historical Properties & Uses
Motherwort is often compared to valerian root. Both herbs promote menstration and exhibit some antidiarrhetic, hypotensive and sedative properties. Older studies concluded motherwort was not as effective as valerian root; but more recent studies have reached the opposite conclusion, rating motherwort's hypotensive action as much as three times as powerful as valerian root. Hypotension and sedation are generally observed in the activity of various and ill-defined glucosides, such as leonurin. Alkaloids, such as leonurinine, are probably responsible for the herb's observed effects on menstruation. The presence of astringent tannins account for motherwort's observed antidiarrheic properties.
These observed experimental properties of motherwort generally support its use as a remedy for nervous heart conditions. More research is needed to assess what, if any, support can be found for use of motherwort to treat gastrointestinal problems such as gas and cramps, menopausal problems, rheumatism, goiter, neuritis, neuralgia, and respiratory ailments.
Sporadic reports of antispasmodic activity could explain some of the herb's gastrointestinal and uterine properties.
Motherwort has no known toxicity, but sensitive people may be allergic.
This herb has approval status by the German Commission E in cardiac disorders and hyperthyroidism.
References:
Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.
Method of Action
Motherwort has hypotensive, sedative and uterine tonic properties
Different investigators, at different times and with slightly different preparations, have reached conflicting conclusions regarding the efficacy of motherwort as a cardiac tonic and hypotensive substance.
The modern motherwort research began in 1930, when Manchurian researchers investigated the pharmacological properties of Leonurus sibiricus, an ancient Chinese species of motherwort closely related to L. cardiacus. They isolated an alkaloid which they called leonurin, and proceeded to determine its effects.
Leonurin caused central paralysis in frogs when injected subcutaneously. Injected into mice, it caused irritation, followed by cramps and finally, respiratory paralysis. Injected into the vein of a cat, it caused a temporary fall in blood pressure, sometimes followed by a slight rise; this seemed to be a peripheral action.
Certain amounts of leonurin were apparently not toxic to heart tissue. In excised frog heart, small doses were slightly stimulating, while large doses were paralysing. In perfusion experiments on toads and rabbits, contraction of the blood vessels was observed in several organs.
A small amount of leonurin injected intravenously into cats quickened the frequency and magnified the amplitude of respiration. An excessive dose however, induced temporary stimulation followed by paralysis and weaker, more irregular respiration. This effect was attributed to the alkaloid's action on the respiratory center.
Leonurin paralyzed the frog's motor nerve endings in a curare-like manner. A small amount of leonurin influenced the excised small intestine of a rabbit in such a way that tonus was regained and the amplitude of the movement magnified, while an excessive dose acted as an inhibitor; the effect was ascribed to the substance's action on the intestinal muscle itself. Tonus of excised rabbit uterus was increased and the amplitude of the movement magnified. Injected into rabbit veins, leonurin caused marked diuretic action.
In 1948, an Italian study investigated leonurus cardiacus and the closely related leonurus marrubiastrum, using the whole plant to prepare ethanol and aqueous extracts. Both plants exhibited mild sedative effects in frogs and rats. The effects were attributed to organic and inorganic components, which were practically insoluble in ethanol. The ethanol extracts had a fleeting depressor effect in the anesthetized dog and a less marked stimulating effect on respiration. L. cardiacus in large doses depressed the isolated frog heart, perhaps because of the K content. Intestine and uterus displayed a very slight stimulation effect. The investigator concluded the plants had no therapeutic value and could not substitute for valerian root.
Years later, utilizing more sophisticated extraction techniques, extracts of motherwort were obtained that exhibited powerful antispasmodic and hypotensive properties. These preparations had sedative effects three times stronger than those of valerian root. Clinical studies also showed antiepileptic activity.
In one study with rabbits, the minimum direct current required to cause bending of the hind leg was determined, both in untreated animals and in those receiving subcutaneous injections of a motherwort extract solution. Trials were made on the sedative action of infusions of motherwort and valerian at different doses. The sedative action of motherwort was one and a half times that of valerian. A mixture of motherwort and valerian at 0.5 ml/kg gave a persistent sedative action.
Using more conventional techniques, another study used liquid extracts of motherwort to obtain the paralysis of the central nervous system of frogs. Contraction of vessels in isolated organs was the reaction to fairly high doses of the concentrated extract. Low doses had no effect on isolated and in situ heart, but high doses decreased the amplitude of contraction. Intravenous injection of the extract sharply decreased blood pressure. Most importantly, lasting hypotension was observed in dogs with experimentally induced hypertension.
Recently, motherwort improved rat myocardial ischemia and mesenteric circulation caused by isoproterenol, reduced heart rate, increased coronary perfusion, and inhibited ADP-induced blood platelet aggregation. It acted more strongly against ADP-induced platelet aggregation than other known herbal inhibitors of platelet aggregation (such as red sage root and ophiopogon root).
In another study, both motherwort and its alcohol extract, K substance, exhibited direct inhibitory action on normal, beating myocardial cells in vitro. K substance was more potent than the whole herb and was able to lower the increased pulsation rate caused by either alpha (neo-synephrine) or beta (isoproterenol) receptor stimulants. This suggests a similar action between K substance and alpha or beta receptor-blocking agents. The action between K substance and calcium chloride varied according to the mode of drug administration. There was inhibitory action when K substance was given prior to CaCl2, but no change occurred when the order was reversed.
Drug Interactions & Precautions
Possible Interactions
Metabolism of motherwort may be decreased by propoxyphene, troleandomycin, para-aminosalicylic acid (PAS), antihistamines, chloramphenicol, disulfiram, halothane, isoniazid, methylphenidate, phenothiazines, and sulfa drugs.
Effects of motherwort may be reduced by propantheline, spironolactone, and triamterene, as well as by antacids, antidiarrheal absorbent suspensions, neomycin, cholestyramine, and other anionic exchange resins. The inotropic action of this herb may also be reduced by propranolol, however it should be noted the effects of the two substances on AV are additive.
Diuretic-induced hypokalemia may increase the activity of motherwort; guinidine, procainamide, and propanodol may also enhance its effect.
Veratrum alkaloids may potentiate the activity of motherwort up to 50%. Motherwort's hypotensive effect may be potentiated by anorectic drugs, such as fenfluramine, whose effects are mediated by brainstem 5HT.
Colchicine may increase sensitivity or enhance the response to motherwort.
The tannin in motherwort may potentiate the antibiotic activity of echinacea. The tannin in motherwort tea may be inactivated by the addition of milk or cream.
Additive effects may occur between the hypotensive property of motherwort and that of dopamine receptor agonists, such as bromocriptine mesylate.
This herb is synergistic with parenteral calcium salts, pancuronium, succinylcholine, rauwolfia alkaloids, ephedrine, epinephrine, and other adrenergic agents.
Motherwort may decrease absorption and diuretic response to furosemide. It may also inhibit the stimulant effect of glucagon on insulin release by Islet of Langerhans cells.
Cyclopropane, or halogenated hydrocarbon anesthetics, may sensitize the myocardium to the cardiotonic effects of motherwort, although the chances are very few of this happening. In addition, this herb should not be used with methotrimeprazine, a potent CNS-depressant analgesic.
Certain antipsychotic drugs (e.g., the phenothiazines), as well as other psychoactive agents which are poorly absorbed in the gastrointestinal tract, may be even more poorly absorbed if motherwort is being used.
Topical application of this astringent herb, in conjunction with the acne product tretinoin (retinoic acid, vitamin A acid), may adversely affect the skin.
Comments
To minimize central nervous system depression and possible synergism, it is wise to avoid using motherwort with procarbazine antineoplastic drugs.
The cardiac alkaloids in motherwort may antagonize the action of heparin. The hypotensive property of motherwort may be additive with the CNS depressant activity of the analgesics nalbuphine HCl and propoxyphene HCl.
Conversely, angina pectoris drugs, such as nadolol and propranolol HCl, may reduce AV conduction induced by this herb.
Certain drugs (e.g., barbiturates, anticonvulsants) induce activity by hepatic microsomal enzymes, which metabolize cardiac glycosides. These agents probably affect the action of motherwort, but in an as yet unknown manner.
In the absence of other hard data, it may be assumed observable interactions occur between the many central nervous system drugs and the psychoactive principles in motherwort.
Safety Factors & Toxicity
No toxicity has been observed from the ingestion of motherwort, but sensitive individuals may incur allergic contact dermatitis from prolonged contact with the plant.
This herb has approval status by the German Commission E.
References:
Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.
Preparation & Administration
Three times a day
Dried herb
2-4 grams
Tea
made from 1 tsp of dried herb
Fluid extract
1:1 in 25% alcohol, 2-4 ml
Tincture
1:5 in 45% alcohol, 3-6 ml
This herb has approval status by the German Commission E.
Recommended daily dosages in Germany are as follows:
4.5 g of the herb.
References:
Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.
Note: This Herbal Preparation information is a summary of data from books and articles by various authors. It is not intended to replace the advice or attention of health care professionals.
References
Am Hospital Formulary Service. Am Soc of Hosp Pharm. Wash, D.C.
Arustamova, F.A. 1963. Hypotensive effects of leonurus cardiaca on animals in experimental chronic hypertension. Izvestiya Academii Nauk Armyanski Ssr, Biologicheski Nauki, 16(7). pp. 47-52.
Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.
Bressler, R., M.D. Bogdonoff & G.J. Subak-Sharpe. 1981. The Physicians Drug Manual. Doubleday & Co, Inc. Garden City, NY. 1213 pp.
Brogan., et.al. 1969. Glucagon therapy in heart failure. Lancet, 1.
Caldwell, J., et.al. 1971. Interruption of the enterohepatic circulation of digitoxin by cholestyramine. Journal of Clin Investigation, 50(12). pp. 2638-2644.
Clark, T.H., A.H. Conney & B.P. Harpole, et.al. 1967. Drug interactions that can affect your patients. Patient Care, 1(11). pp. 33-71.
Cohen, M.S. 1970. Therapeutic Drug Interactions. University of Wisconsin Medical Center. Madison, WS.
Committee on Pharmocopaeia of the Am Institute of Homeopathy, The Homeopathic Pharmacopaeia of the United States. 8th ed., Vol 1. Otis Clapp and Son, Agents, Boston, l981.
DeMonts, H. & S.H. Rahimtoola. 1977. Digitalis and propranolol - together. Modern Medicine, 45(8). pp. 68-69, 75, 79.
Drug package insert (FDA approved official brochure) and other labeling based on sponsored clinical investigations and New Drug Application data.
Erspammer, V. Ricerche farmacologiche sul leonurus cardiaca L. (e sul leonurus marrubiastrum l.) Archiv. Intern. Pharmacodynamie, 76, 132-152, 1948.
Fann, W.E. 1973. Chlorpromazine - effects of antacids on its gastrointestinal absorbtion. J of Clin Pharm, 13(10). pp. 388-90.
Fann, W.E., et.al. 1973. The effects of antacids on the blood levels of chlorpromazine. Clin Pharmacology and Therapeutics, 14(1-2). p. 135.
Frey, H.H. & E. Kampmann. 1966. Interaction of amphetamine with anticonvulsant drugs. II. Effect of amphetamine on the absorption of anticonvulsant drugs. Acta Pharmachologic et Toxicologica, 24. p. 310.
Goodman, L.S. & A. Gilman. 1975. Pharm Basis of Thera. MacMillan, NY.
Green, R. & C.C. Oliver. 1968. Sensitivity to propranolol after digoxin intoxication. British Medical Journal, 3. pp. 404-413.
Hansten, P.D. 1979. Drug Interactions, 4th ed. Lea & Febiger, Phila.
Hyde, F.F. British Herbal Pharmacopoeia. British Herbal Medicine Assoc: West Yorks, England, 1983
Isaev, I. & M. Bojadzieva. Obtaining galenic and neogalenic preparations and experiments for the isolation of an active substance from leonurus cardiaca. Nauchni Trudy Visshiya Med. Inst. Sofiya, 37(5), 145-152, 1960.
Jenkins, L. 1968. The interaction of drugs. Canadian Anaesthesiologists Society Journal, 15(3). pp. 111-117.
Karlin, J.M. & H. Kutt. 1970. Acute diphenylhydantoin intoxication following halothane anesthesia. Journal of Pediatrics, 76. p. 941.
Kastrup, E.K., ed. 1981. Drug Facts and Comparisons, 1982 edition. Facts and Comparisions Division, J.P. Lippincott Co, Phila(St. Louis).
Kubota, S. & S. Nakashima. The study of leonurus sibiricus, L. I.Chemical study of the alkaloid (leonurin) isolated from leonurus sibiricus, L. Nippon Yakugaku Zasshi, 11(2), 153-158, 1930, Brevaria 10, 1930.
Kubota & Nakashima. The study of leonurus sibericus L. II. Pharmacological study of the alkaloid leonurin isolated from leonurus sibericus L. Nippon Yakugaku Zasshi, 11(2), 159-167, Brevaria, 11-2, 1930.
Kutt, H., et.al. 1968. Inhibition of diphenylhydantoin metabolism in rats and rat liver microsomes by antitubercular drugs. Neurology, 18.
Levine, W.G. 1970. Heparin and oral anticoagulants. The Pharmacological Basis of Therapeutics, 4th ed. Goodman, L.S. & A. Gillman, eds. MacMillan, New York.
Lindenbaum, J., et.al. 1972. Impairment of digoxin absorption by neomycin. Clin Research, 20. p. 410.
List, P. & L. Hoerhammer. 1969-1976. Hagers Hanbuch der Pharmazeutischen Praxis, vols. 2-5. Springer-Verlag, Berlin.
Martin, E.W. 1978. Drug Interactions Index, 1978/79. J.B. Lippincott Company, Philadelphia.
Meek, W.J., H.R. Hathaway & O.S. Orth. 1937. The effects of ether, chloroform and cyclopropane on cardiac automaticity. Journal of Pharmacology and Experimental Therapeutics, 61. pp. 240-252.
Morrelli, H.F. & K.L. Melmon. 1968. The clinician's approach to drug interactions. California Medicine, 109(11). pp. 380-389.
Mowrey, Daniel B., Ph.D. Exper. Psych., Brigham Young University. Director of Nebo Institute of Herbal Sciences. Director of Behavior Change Agent Training Institute. Director of Research, Nova Corp.
Nagata, R. 1969. Drug interactions -- digitalis glycosides and kaliuresis. Hospital Form Management, 4(8). pp. 30-32.
Olesen, O.V. 1966. Disulfiram (antabuse) as inhibitor of phenytoin metabolism. Acta Pharmacologica et Toxicologica, 24. p. 317.
Rose, J.Q., et.al. 1977. Intoxication caused by interaction of chloramphenicol and phenytoin. J of the Am Med Assoc, 237. p. 2630.
Scientific Committee, British Herbal Pharmocopaeia, British Herbal Med Assoc, Lane House, Cowling, Na Keighley, West Yorks, Bd Bd220lx, l983.
Sherrod, T.R. 1967. The cardiac glycosides. Hosp Pract, 2. p. 56.
Siris, J.H., et.al. 1974. Anticonvulsant drug-serum levels in psychiatric patients with seizure disorders. NY St J of Med, 74 p.1554.
Smith, J.W. 1966. Manual of Medical Therapeutics, 19th ed. Little, Brown & Co., Boston. pp. 85-91.
Vincent, D. & G. Segonzac. 1953. Comptes Rendus des Seances de la Societe de Biologie et de ses Filiales, 147. pp. 1776-1779.
Walton, R.P. 1965. "Cardiac glycosides II: pharmacology and clinical use. V.A. Drill, ed. Pharmacology in Medicine, 3rd ed.. McGraw Hill. New York.
Yano, S. The corticoid-like actiion of glycyrrhizin. Nippon Nabinpi Gakkai Zasshi, 34, 745-751, 1958.
Zhang, C., et.al. Studies on actions of extract of motherwort. Journal Of Traditional Chinese Medicine, 2(4), 267, 1982.
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Leonurus cardiaca
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