Botanical Description & Habitat
Asthma weed Bladderpod Gag root Indian tobacco Pukeweed Vomit wort
Found in meadows, woods, and grassy places throughout the United States.
The plant can grow from six inches to three feet in height, and has an angular, hairy, yellowish-green stem. The pale green leaves are alternate, oblong, hairy, and have irregularly toothed margins. Small, pale blue flowers grow in loose racemes from July to November. The fruit is a two-celled capsule containing ovate-oblong, light brown seeds.
Herb - dried, gathered just after flowering
Historical Properties & Uses
Lobelia was first introduced into medicine as an emetic by Mannasse Gutler in 1775; thereafter it was used extensively by Dr. Samuel Thompson and his followers. It was employed to cure asthma as early as 1809, but the first important pharmacological study of the herb was not performed until 1875.
This work, and several papers that followed, indicated lobelia markedly stimulated respiration, increasing both depth and rate; the effect lasted longer if the vagi were intact than if they were cut. The herb also dilated the vagi, which would explain its beneficial action in asthma.
Lobelia's unpleasant side effects, such as vomiting, were well-known, and precluded use of crude preparations of lobelia as a respiratory stimulant; in fact, overdoses were found to paralyze respiration. Thus, for a considerable time during the early part of this century, the plant was not often used in research or in medical practice.
Heinrich Wieland separated lobelia's alkaloids in 1921; studies by him and his colleagues led to renewed interest in the herb, specifically in the use of one of its alkaloids (alpha lobelin), whose action closely resembled the whole plant extract, except it did not possess the unpleasant emetic effect.
Subsequently, alpha-lobelin was introduced into clinical medicine as a specific respiratory stimulant, and it was used with considerable success in collapse, various types of drug poisoning, and asphyxia neonatorum. The drug was intensely investigated as an emergency respiratory stimulant and compared to scores of similar substances. The general consensus was lobelin acted directly on the heart muscle itself.
Lobelin and lobelia fell into disuse as the popularity of synthetic drugs grew. Attempts to revive its popularity, as a smoking deterrent for example, were usually met with little enthusiasm by the producers of proprietary drugs.
Despite experimental evidence of its efficacy, the oft-encountered side effects of early experiments and clinical studies were cited as reason to avoid use of lobelia and its derivatives. The general pharmacology of lobelia may or may not be similar to its major constituents, lobeline and alpha-lobelin.
Lobeline is hypertensive and hypotensive; it stimulates cardiovascular parameters, induces bradycardia, and blocks the neuromuscular junction. It produces apnea, emesis, and anesthesia. It suppresses the appetite, inhibits or stimulates the gastrointestinal system, and inhibits platelet aggregation.
The properties of lobeline support the following uses for lobelia: as an anti-asthmatic, emetic, smoking deterrent, and expectorant. Such qualities oppose the reported gastrointestinal antispasmodic and nervine actions of the whole plant.
Method of Action
The pharmacology of lobeline is fairly well known; its sulphate was a popular ingredient in proprietary preparations designed to help smokers kick their habit. Research on such medicines never clearly proved them effective, yet even today there are anti-smoking pills on the market containing lobeline.
Lobeline hydrochloride has been used as a respiratory stimulant to counter respiratory failure from diseases, drowning or other accidents, and from narcotic or CO2 poisoning. An injection of lobeline hydrochloride has been used to resuscitate newborns.
The pharmacological actions of lobeline are: hypertension/hypotension; cardiovascular stimulation; bradycardia and bradyarrhythmia; carotid body stimulant; neuromuscular blockade; anesthetic; ganglionic stimulant; apnea/hyperpnea; anti-asthmatic; gastrointestinal inhibition/stimulation and appetite suppressant; adrenal stimulation; emetic; smoking deterrent; and platelet aggregation inhibition.
Lobeline first excites, then depresses the central nervous system. In low doses, it dilates the bronchioles and increases respiration; high doses depress respiration (apnea), and cause profuse sweating, brachycardia, and hypotension.
The main effects of lobelia are apnea, bradycardia, and hypotension. In human subjects, at high dose of 1.0 mg and low dose of 0.5 mg, lobeline produced apnea with and without cough in 12 of 15 patients. The cough response was replaced with apnea as the dosage decreased. It did not produce a sensation of breathlessness. Stimulation of the pulmonary receptors with lobeline (in the absence of cough) did not produce any of the typical cardiovascular effects, such as hypotension and bradycardia, observed in cats and rabbits. Other studies, however, have observed both hypotension and bradycardia during lobeline-induced "ventilatory depression" in man. Differences in dosage probably account for the differences in observations.
The lobelia plant has not been studied nearly as much as its constituent, lobeline. Lobelia's role as a potential smoking deterrent, however, has been the subject of clinical study for a hundred years; its alternate name is Indian tobacco, and its emetic effect is well substantiated.
The first demonstration of the herb's ability to induce hypotension and bradycardia was made with a crude extract of lobeline, administered intravenously. But it had already been observed lobelia markedly stimulated respiration, increasing both depth and rate. The herb also displayed a broncho-dilator action. These findings help explain why lobelia is effective in asthma.
Injections of crude lobelia extracts caused a lowering of blood pressure and a fall in heart rate.
In a study comparing the effects of lobelia and those of lobeline on the frog's heart, considerable differences were noted. Lobelia extract caused arrhythmia, decrease in systole, and reduction of the number of contractions per minute. Lobeline had none of those actions.
Generally, lobelia's active alkaloids are divided into alpha-, beta-, and gamma-lobelines, plus lobelamine and lobelamidine. Alpha-lobelin is most often used in basic research. In normal animals, alpha-lobelin displays no emetic action, nor stimulation of the autonomic nerve endings, although these actions are characteristic of the amorphous alkaloids of the plant.
Fatal intravenous doses produce almost simultaneous cessation of respiration and heartbeat after short clonic convulsions, followed by flaccid paralysis. In rabbits, the drug is rapidly destroyed. Alpha-lobelin, like lobelia extracts, produces several types of medullary stimulation (vomiting, convulsions, and blood pressure and respiratory changes). In human patients suffering from morphine or barbituate poisoning (or a combination of the two), carbon monoxide poisoning, or increased intracranial pressure, alpha-lobelin produces either no appreciable stimulation of the respiration, or only a slight transient stimulation. As a therapeutic agent, the pharmacological properties of alpha-lobelin do not differ essentially from those of the amorphous alkaloids or extracts of lobelia.
Lobelia is probably not a euphoriant
In recent years, lobelia has gained a reputation as a euphoriant, and is smoked like marijuana. It is often combined with other potentially psychoactive plants to achieve a "legal" high. There is no research to support this claim.
Lobelia has some antibiotic action
Lobelia has some antibiotic activity against gram negative and gram positive bacteria.
Drug Interactions & Precautions
Lobelia should be used with caution in conjunction with CNS-depressants or stimulants. The nicotinic activity of this herb may antagonize the effects of heparin.
Lobelia may increase the metabolism of digitoxin, oral contraceptives, phenytoin, corticosteroids, fluroxene, methadone, metyrapone, and tetracyclines. The metabolism of lobelia may be increased by barbiturates ethanol, diazoxide, loxapine, and vitamin B-6. Conversely, the herb's metabolism may be decreased by propoxyphene, troleandomycin, para-aminosalicylic acid (PAS), antihistamines, chloramphenicol, disulfiram, halothane, isoniazid, methylphenidate, phenothiazines, and sulfa drugs.
Lobelia's diuretic action may reduce renal clearance of lithium. It should be noted the use of diuretics may require dosage adjustments of antidiabetic drugs.
Lobelia may decrease absorption and diuretic response to furosemide, and may also inhibit glucagon's stimulant effect on insulin release by Islet of Langerhans cells.
The lobeline in lobelia increases acetylcholine response; the herb may therefore potentiate the effects of cholinergic drugs.
The anti-inflammatory activity of the herb can be seriously inhibited by phenobarbital and certain other sedatives and hypnotics, such as chloral hydrate and meprobamate. This is also true of beta-adrenergic blocking agents, such as propanolol.
To minimize central nervous system depression and possible synergism, lobelia should not be taken by persons on procarbazine antineoplastic drugs.
The neuromuscular-relaxant action of the herb may be enhanced by the use of certain aminoglycoside antibiotics, such as clindamycin.
Prolonged use of this diuretic herb may affect certain laboratory test results, such as electrolytes (especially potassium and sodium), blood urea nitrogen (BUN), uric acid, glucose, and protein bound iodine (PBI).
Safety Factors & Toxicity
Lobelia has strong emetic properties. Use extreme caution when ingesting it in any form, especially fresh or as tincture.
Ingestion of 50 mg of dried herb or 1 ml of lobelia tincture may cause severe symptoms in some people, including: dryness of the throat, nausea, vomiting, diarrhea, abdominal pains, muscular twitching, rapid pulse, labored respiration and constricted pupils nonreactive to light. Convulsions eventually occur, followed by respiratory death.
The intraperitoneal LD50 of lobeline in mice is 40 mg/kg; subcutaneous LD50 is 37 mg/kg; intravenous LD50 is 6 mg/kg.
Lobeline, the herb's active component, resembles nicotine in action and in toxicity, although it is not as potent in stimulation and paralysis of the sympathetic ganglion cell.
Preparation & Administration
Three times a day
Some individuals may be unusually sensitive, so start with smallest dosages.
made from 1/8 tsp of dried herb
1:1 in 50% alcohol, 0.2-0.6 ml
1:8 in 60% alcohol, 1-4 ml
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.
Am Hospital Formulary Service. Am Soc of Hosp Pharm. Wash, D.C.
Bevan, J.A. & M. Verity. Action of lobeline on intrathoracic receptors: a comparison with phenlydiguanide, serotonin and veratridine. J Of Pharm And Exper Ther, 132(1), 42-49, 1961.
Bjoerkman, S. Role de la lobeline sur les contractions parasympathiques des muscles bronchiques. Comptes Rendus Societe Biologie, 94(12), 947-948, 1926.
Bjoerkman, S.E. Action de la lobeline sure l'innervation parasympathique de l'intestin. Comptes Rendus Societie Biologie, 94(12), 945-946, 1926.
Boston Collaborative Drup Surveillance Program. 1972. Tetracycline and drug-attributed rises in blood urea nitrogen. J of Am Med Assoc, 220.
Bressler, R., M.D. Bogdonoff & G.J. Subak-Sharpe. 1981. The Physicians Drug Manual. Doubleday & Co, Inc. Garden City, NY. 1213 pp.
Brodie, T.G. Journal Of Physiology, 24, 169, 1903.
Brogan, E., et.al. 1969. Glucagon therapy in heart failure. Lancet, 1. pp. 482-484.
Cambar, P.J., S.R. Shore & D.M. Aviado. Bronchopulmonary and gastro-intestinal effects of lobeline. Arch Int Pharmacodyn, 177(1), 1969.
Chambers, G., R.J. Kerry & G. Owen. 1977. Lithium used with a diuretic. British Medical Journal, 2. pp. 805-806.
Chiles, V.K. 1968. Drug interactions and the pharmacist. Canadian Pharaceutical Journal, 101(7). pp. 241-247.
Claeson, B. & L. Bachmann. Comptes Rendus Societe De Biologie, 42, 638, 1925.
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.
Clementi, A. Arch. Fuer Experimentalle Path. Und Pharmakolog., 181, 265, 1936.
Committee on Pharmocopaeia of the Am Institute of Homeopathy, Homeopathic Pharm of U.S. 8th ed., Vol 1. Otis Clapp & Son, Agents, Boston, l981.
Cooper, P. Poisoning By Drugs And Chemicals, Plants And Animals, 3rd Edition, Year Book Medical Publishers, Chicago, 1974.
D'Amico, M.L. Richere sulla presenza di sostanze ad azione antibiotica nelle piante superiori. Fitoterapia, 26(1), 77-79, 1950.
Davison, G.C. & R.C. Rosen. Lobeline and reduction of cigarette smoking. Psychological Reports, 31, 443-456, 1972.
Dixon, W.E. Heffter's Handbuch Der Experimentellen Pharmacologie, 1924, II, 2, 719.
Dollery, C.T. 1965. Physiological and pharmacological interactions of antihypertensive drugs. Procs of Royal Soc of Med, 58(11) p.983-987.
Drug package insert (FDA approved official brochure) and other labeling based on sponsored clinical investigations and New Drug Appli. data.
Edmunds, C.W. American Journal Of Physiology, 11, 79, 1904.
Franken, H. Darstellung der wirkung des lobelins und der kohlensaeure auf die atmung des menschen in der narkose. Klin. Wochenschrift, 8(10), 439-442, 1929.
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.
Gad, R.E.A, S. Clayman & D. Hebert. Effect of lobeline on guinea pig platelet aggregation induced by adenosine diphosphate, collagen and thrombin. Pharmacolo. Research Comm, 3(3), 279-286, 1971.
Goldner, M.G., H. Zarowitz & S. Akgun. 1960. Hyperglycemia and glycosuria due to thiazide derivatives administered in diabetes mellitus. New England Journal of Medicine. 262(Feb 2). pp. 403-405.
Goodman, L.S. & A. Gilman. 1975. Pharm Basis of Thera. Macmillan, NY.
Haeger, K. Long-Term Study of Intermittent Claudication and Tocopherol. Annals Of The New York Academy Of Sciences, 393 (1982).
Hansen, J. et.al. 1966. Dicumarol-induced diphenylhydantoin intoxication. Lancet, 2. p. 265.
Hansten, P.D. 1968. Antidiabetic drug interactions. Hospital Form. Management, 4(2). pp. 30-32.
Hansten, P.D. 1979. Drug Interactions, 4th ed. Lea & Febiger, Phila.
Houssay, B.A. & E.A. Molinelli. Effect of nicotin, cytisin, lobelin, coniin, piperidin and quaternary ammonias on adrenal secretion. Journal Of Physiology, 76(3), 551-576, 1926.
Hurtig, H.I. & W.L. Dyson. 1974. Lithium toxicity enhanced by diuresis. New England J of Med, 290(Mar 28). pp. 748-749.
Hyde, F.F. British Herbal Pharmacopoeia. British Herbal Medicine Assoc: West Yorks, England, 1983
Jain, S.K., S. Subramanian, D.B. Julka & A. Guz. Search for evidence of lung chemoreflexes in man: study of respiratory and circulatory effects of phenyldiguanide and lobeline. Clin Sci, 42, 163-177, 1972.
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).
Kelkar, V.V., R.S. Gupta & S.V. Gokhale. The isolated dremaster muscle preparation and (external) spermatic nerve-cremaster muscle preparatiion of the guinea-pig. J Of Pharm & Pharm, 28, 290-293,1976.
Klide, A.M. & D.M. Aviado. Carotid receptors and bronchomotor responses. Archives Of Environmental Health, 17(7), 65-70, 1968.
Konzett, H. 1951. Pharmacology of lobeline. Archiva Internationale Pharmacodynamica et Therapia, 85(3/4). pp. 446-450.
Korczyn, A.D., I. Bruderman & K. Braun. Cardiovascular effects of lobeline. Arch. Int. Pharmacodyn., 182(2), 370-375, 1969.
Kutt, H., et.al. 1968. Inhibition of diphenylhydantoin metabolism in rats and rat liver microsomes by antitubercular drugs. Neurology, 18.
Laffan, R.J. & H.L. Borison. Emetic action of nicotine and lobeline. J Of Pharm And Exper Thera, 121(4), 468-476, 1957.
List, P. & L. Hoerhammer. 1969-1976. Hagers Hanbuch der Pharmazeutischen Praxis, vols. 2-5. Springer-Verlag, Berlin.
London, S.J. Clinical evaluation of a new lobeline smoking deterrent. Current Thera Rsrch. Clin & Experi, 5(4), 167-175, 1963.
Lutz, E.G. 1975. Lithium toxicity precipitated by diuretics. Journal of the Medical Society of New Jersey, 72(5). pp. 439-440.
Mansuri, S.M., V.V. Kelkar & M. Jindal. Actions of lobeline and sparteine on neuromuscular junction. Indian Journal Of Medical Research, 62(6), 930-937, 1974.
Mansuri, S.M., V.V. Kelkar & M.M. Jindal. Some pharmacological characteristics of ganglionic activity of lobeline. Arzneimittel-forschung, 23(12), 1721-1725, 1973.
Martin, E.W. 1978. Drug Interactions Index, 1978/79. J.B. Lippincott Company, Philadelphia.
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.E. 1969. Drug interactions -- digitalis glycosides and kaliuresis. Hospital Form Management, 4(8). pp. 30-32.
Norris, V.H. & S. Weiss. The pharmacological and therapeutic properties of alpha-lobelin. A comparison of its action on the respiratory center with that of other respiratory stimulants. J Of Pharmacology And Experimental Therapeutics, 31(1), 43-64, 1927.
Olesen, O.V. 1966. Disulfiram (antabuse) as inhibitor of phenytoin metabolism. Acta Pharmacologica et Toxicologica, 24. p. 317.
Ott, L. Philadelphia Med. Times, 6, 121, 1875.
Rapp, G.W., B.T. Dusza & L. Blanchet. Absorption and utility of lobeline as a smoking deterrent. Am J Of The Med Sci, Mar, 1959.
Riesterer, L. & R. Jaques. 1968. Interference by beta-adrenergic blocking agents with the antiinflammatory action of various drugs. Helv Physiol Acta, 26. pp. 287-293.
Rose, J.Q., et.al. 1977. Intoxication caused by interaction of chloramphenicol and phenytoin. J of the Am Med Assoc, 237. p. 2630.
Salem, H., M. Penna & D.M. Aviado. Mechanism for bradycardia arising from stimulation of carotid bodies. Arch. Int. Pharmacodyn. 150(1-2), 249-255, 1964.
Scientific Committee, British Herbal Pharmocopaeia, British Herbal Med Assoc, Lane House, Cowling, Na Keighley, West Yorks, Bd Bd220lx, l983
Siris, J.H., et.al. 1974. Anticonvulsant drug-serum levels in psychiatric patients with seizure disorders. NY St J of Med, 74 p.1554.
Stuart, D.M. 1968. Drug metabolism Part 2. Drug interactions. PharmIndex, 10(10). pp. 4-16.
Thorn, G.W. 1966. Clin considerations in the use of corticosteroids. New England J of Medicine, 274(Apr 7). pp. 775-781.
Tuttle, C.B. 1969. Drug interactions. Can J of Hosp Pharm, 22(5-6).
Whitehead, R.W. & D.C. Elliott. Electrocardiographic studies of the action of alpha lobelin and epinephrine on the mammalian heart. J Of Pharm And Experi Therap, 31(2), 145-176, 1927.
Whitehouse, M.W., P.D.G. Dean & T.G. Halshall. Uncoupling of oxidative phosphorylation by glycyrrhetic acid, fusidic acid and some related triterpenoid acids. J Of Pharm And Pharm, 19(8), 533-544, 1967.
Wieland, H. & R. Mayer. Arch. Exper. Path. Und Parm., WXCII, 169, 1922.
? Southwest School of Botanical Medicine
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