DOCSLIB.ORG

Effect of Amitriptyline Antidotes on Repetitive Extrasystole Threshold

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Effect of Amitriptyline Antidotes on Repetitive Extrasystole Threshold Effect of amitriptyline antidotes on repetitive extrasystole threshold The effect ofamitriptyline that leads to ventricular tachycardia was evaluated hy the repetitive extrasystole threshold (RET) technique in 18 dogs. The RET was 28.8 ± 7.9 mamp before and 8.2 ± 5.3 mamp after amitriptyline. p < 0.001. Physostigmine. propranolol. sodium bicarbonate, and left stellate ganglionectomy reversed the effect of amitriptyline on RET. We conclude that amitriptyline overdose predisposes to sudden death by lowering the ventricular fibrillation threshold. This cardiotoxic effect is mediated partly through the central nervous system and can be inhibited by increased plasma binding (bicarbonate), cholinergic stimulation (physostigmine), beta adrenergic blockade (propranolol), and sympathetic denervation (left stellate ganglionectomy). Jonathan M. Tobis, M.D., and Wilbert S. Aronow, M.D. Irvine, Calif. Cardiology Section and Medical Service, University of California, Irvine, and Long Beach Veterans Administration Medical Center The mechanism of tricylic antidepressant ac­ tyline on the repetinve extrasystole threshold tion is not established. The cardiotoxic proper­ (RET), Matta et al." have shown that the RET ties have been established.?- II, 14 The most was a good marker of the ventricular fibrillation common serious clinical arrhythmia is ventricu­ threshold in 91% of the animals they studied. A lar tachycardia." Several antidotes have been single repetitive extrasystole occurred when reported as successful in reversing the central 66% of the fibrillation current was delivered, nervous system and cardiac manifestations oftri­ and repeated extrasystoles were induced at 82% cyclic antidepressant overdose, i.e., physo­ of the fibrillation current. stigmine, propranolol, and sodium bicarbon­ We then explored the effect of several poten­ ate,3-5, 10. 12. I:l but there is no agreement on tial antidotes. To elucidate the mechanism of their mechanism of action or efficacy. I, 2 action of the tricyclics, we manipulated sympa­ We investigated some of the cardiotoxic thetic and parasympathetic nervous system ac­ properties of amitriptyline. Because of the life­ tivity with physostigmine and propranolol and threatening effects of an overdose in humans, by cutting the left stellate ganglion. We also we thought we were limited to the animal model studied the effect of sodium bicarbonate, to analyze the effect of an overdose of amitrip- Methods Eighteen healthy mongrel dogs of both sexes, Received for publication Oct. 26, 1979. weighing 16 to 27 kg, were used. Anesthesia Accepted for publication Dec. 8. 1979. was induced intravenously with sodium thi­ Reprint requests to: Jonathan M. Tobis, M.D., Assistant Profes­ amylal 4 mg/kg and alpha chloralose 40 to 80 sor of Medicine, University of California, Irvine, !OI City Dr. So., Orange, CA 92668. mg/kg at a concentration of 5 mg/ml in heated 602 Volume 27 Antidotes to amitriptyline poisoning 603 Number 5 normal saline. Additional alpha chloralose 20 to ments of I or 2 mamp until there was a repeti­ 50 mg/kg was given if required during the ex­ tive extrasystole. The RET was defined as the periment to maintain anesthesia. The dogs were current required to induce at least one extra de­ intubated and ventilated with a Harvard pump polarization after the premature electrical input. with a mixture of room air and 100% oxygen. The RET was verified by obtaining extrasys­ The ventilator was adjusted to stabilize the ar­ toles in at least 2 of 3 trials. The maximum terial blood pH at 7.30 to 7.45. Overhead lights output of our generator was 40 mamp. were used to maintain body temperature. A 16 F Experimental interventions. After the base­ polyethylene catheter was inserted percutane­ line RET was obtained and reproduced 15 to 30 ously into the right femoral vein for drug admin­ min later, amitriptyline was given as a bolus istration. The left femoral artery was cannulated infusion of 10 to 20 mg/kg over 30 min in 9 percutaneously with a 16 F polyethylene cathe­ dogs. In 7 other dogs an amitriptyline bolus of 3 ter and used to measure systemic blood pressure to 10 mg/kg was injected intravenously and fol­ and obtain arterial blood samples. A Statham D lowed by a constant infusion of 0.015 to 0.025 23 De transducer and a Grass Polygraph re­ mg/kg/min. The RET was obtained IS min corder model 7 were used to record systemic after the initial bolus of amitriptyline and was blood pressure. An electrocardiogram was re­ verified as stable up to 60 min later. corded on the Grass Polygraph using a standard In 6 dogs physostigmine was given intrave­ limb lead. nously as a 2-mg bolus 30 to 45 min after the Electrical testing of the heart was performed amitriptyline bolus or during continuous ami­ as follows. The chest cavity was opened by triptyline infusion. Another RET was obtained right thoracotomy. A midline sternotomy was 10 to IS min after physostigmine. performed in the series of left stellate gan­ In 5 dogs propranolol 2 mg was given intra­ glionectomy experiments. Two Cordis suture­ venously 30 to 45 min after the amitriptyline less epicardial electrodes, model 324-856, were bolus or during continuous amitriptyline infu­ placed 2 em apart on the right ventricle midway sion. The RET was determined 10 to IS min between the apex and the atrioventricular after propranolol. groove. The electrodes were connected through In 5 dogs a midline sternotomy was per­ a stimulus isolation unit (Grass SIU-5A) and a formed. The RET was determined at baseline constant-current unit (Grass CCU-2A) to a and then during an amitriptyline infusion of Grass S-44 square-wave pulse generator. The 0.015 to 0.025 mg/kg/min after an initial intra­ output of this assembly was calibrated with an venous bolus of 3 to 10 mg/kg. A left stellate oscilloscope. The pulse generator was set at 200 ganglionectomy was performed through the bpm to overcome any tachycardia induced by sternotomy incision. During constant infusion the anticholinergic effect of amitriptyline. The of amitriptyline the RET was again obtained. heart was paced with a 2-msec impulse. The In 2 dogs sternotomy was performed, fol­ pulse generator had the ability to deliver a pre­ lowed by baseline determination of RET. These mature impulse with variable delay after the last dogs then had a left stellate ganglionectomy paced beat. The pulse generator would then shut prior to any drug administration. After the off for 3 sec, during which the effect of the postganglionectomy RET was performed, an premature extrastimulus could be observed on amitriptyline bolus of IS mg/kg was followed the electrocardiogram. by a 0.015- or 0.025-mg/kg/min infusion in­ The RET was obtained in the manner de­ travenously, and RET was repeated. scribed by Matta et al.? Electrical diastole was In 4 dogs RET was determined before and scanned in 5-msec decrements, beginning at the during intravenous amitriptyline infusion. RET end of the T wave and ending at the border of was repeated after 44 mEq sodium bicarbonate the strength interval curve, i.e., where no de­ was given intravenously over 5 min. Arterial polarization could be induced with the extrasys­ pH was determined before and after bicarbonate tole. The current of the extrasystole impulse while RET was being determined. was set at 2 mamp and was increased in incre- Several amitriptyline blood samples were 604 Tobis and Aronow Clin. Pharmacal. Ther. May 1980 40 40 36 36 32 32 28 28 24 24 ""E 20 20 -c E 16 16 12 12 Control Amitriptyline Physostigmine Control Amitriptyline Propranolol Fig. 1. Repetitive extrasystole threshold before Fig. 2. Repetitive extrasystole threshold before amitriptyline, after amitriptyline, and after physo­ amitriptyline, after amitriptyline, and after proprano­ stigmine. rnA, Milliampere (mamp). lol. rnA, Milliampere (mamp). drawn during each experiment to ensure ade­ triptyline followed by left stellate ganglionec­ quate toxic blood levels. Amitriptyline and tomy. Mean RET was 28.4 ± 7.5 mamp before nortriptyline plasma levels were determined by and 9.4 ± 3.8 mamp after amitriptyline, p < Bio-Science Laboratories. 0.005, and 27.6 ± 9.8 mamp after left stellate ganglionectomy (control not significantly dif­ Results ferent). For the entire group of 16 dogs RET ± 1 SD Fig. 4 shows RET in the 4 dogs given ami­ was 28.8 ± 7.9 mamp during the control pe­ triptyline followed by sodium bicarbonate. riod and 8.2 ± 5.3 mamp after amitriptyline, Mean RET was 25.3 ± 4.0 mamp before and p < 0.001. Average blood level at the time of 5.8 ± 3.3 mamp after amitriptyline, p < 0.01, RET determination was 933 ± 562 ng/ml. and 21.3 ± 16.0 mamp after sodium bicarbon­ Fig. 1 shows RET in the 6 dogs given ami­ ate (control not significantly different). Mean triptyline followed by physostigmine. Mean arterial pH was 7.26 ± 0.08 before and 7.39 ± RET was 23.5 ± 5.7 mamp before and 9.8 ± 0.08 after an average dose of 44 mEq sodium 6.0 rna after amitriptyline, p < 0.001, and bicarbonate. 26.7 ± 6.8 mamp after physostigmine (control In the 2 dogs with left stellate ganglionec­ not significantly different). tomy before amitriptyline infusion, the ventricu­ Fig. 2 shows RET in the 5 dogs given ami­ 1M fibrillation threshold (VFT) was measured triptyline followed by propranolol. Mean RET directly rather than RET, because ventricu­ was 35.6 ± 6.1 mamp before and 5.0 ± 5.2 lar fibrillation developed in the control periods mamp after amitriptyline, p < 0.001, and during RET measurement. Control VFT was 38.0 ± 2.8 mamp after propranolol (control not 33.0 ± 7.5 mamp before and 37.0 ± 0.0 significantly different).
Load more

Recommended publications
  • Comparing the Effect of Venlafaxine and the Combination of Nortriptyline and Propranolol in the Prevention of Migraine
    Comparing the Effect of Venlafaxine and the Combination of Nortriptyline and Propranolol in the Prevention of Migraine Arash Mosarrezaii1, Mohammad Reza Amiri Nikpour1, Ata Jabarzadeh2 1Department of Neurology, Imam Khomeini Hospital, Urmia University of Medical Sciences, Urmia, Iran, 2Medical Student, Urmia University of Medical Sciences, Urmia, Iran Abstract Background: Migraine is a debilitating neurological condition, which can be categorized into episodic and chronic groups based on its clinical pattern. Avoiding the risk factors exacerbating migraine is not enough to reduce the frequency and severity of migraine headaches, and in the case of non-receiving proper drug treatment, episodic migraines have the potential to become chronic, which increases the risk of cardiovascular complications RESEARCH ARTICLE and leaves great impact on the quality of life of patients and increasing the health-care costs. The objective of this research was to compare the effects of venlafaxine (VFL) and nortriptyline and propranolol in preventing migraines. Methods: This research is an interventional study performed on 60 patients with migraine admitted to the neurological clinic. Patients were visited at 3 time intervals. In each stage, the variables of headache frequency, headache severity, nausea, vomiting, and drowsiness were recorded. Data were analyzed using SPSS 23 software. Results: VFL drug with a daily dose of 37.5 mg is not only more tolerable in the long term but also leaves better effect in reducing the frequency and severity of headaches compared to the combination of nortriptyline and propranolol. Conclusion: VFL is an appropriate, effective, and tolerable alternative to migraine treatment. Key words: Migraine, nortriptyline, propranolol, venlafaxine INTRODUCTION Patients with CM are less likely to have full-time job than patients with episodic type, and they are at risk of job igraine is known as a common incapacity, anxiety, chronic pain, and depression 2 times neurological disorder and causes more than patients with episodic migraine.
    [Show full text]
  • Schizophrenia Care Guide
    August 2015 CCHCS/DHCS Care Guide: Schizophrenia SUMMARY DECISION SUPPORT PATIENT EDUCATION/SELF MANAGEMENT GOALS ALERTS Minimize frequency and severity of psychotic episodes Suicidal ideation or gestures Encourage medication adherence Abnormal movements Manage medication side effects Delusions Monitor as clinically appropriate Neuroleptic Malignant Syndrome Danger to self or others DIAGNOSTIC CRITERIA/EVALUATION (PER DSM V) 1. Rule out delirium or other medical illnesses mimicking schizophrenia (see page 5), medications or drugs of abuse causing psychosis (see page 6), other mental illness causes of psychosis, e.g., Bipolar Mania or Depression, Major Depression, PTSD, borderline personality disorder (see page 4). Ideas in patients (even odd ideas) that we disagree with can be learned and are therefore not necessarily signs of schizophrenia. Schizophrenia is a world-wide phenomenon that can occur in cultures with widely differing ideas. 2. Diagnosis is made based on the following: (Criteria A and B must be met) A. Two of the following symptoms/signs must be present over much of at least one month (unless treated), with a significant impact on social or occupational functioning, over at least a 6-month period of time: Delusions, Hallucinations, Disorganized Speech, Negative symptoms (social withdrawal, poverty of thought, etc.), severely disorganized or catatonic behavior. B. At least one of the symptoms/signs should be Delusions, Hallucinations, or Disorganized Speech. TREATMENT OPTIONS MEDICATIONS Informed consent for psychotropic
    [Show full text]
  • Selective Labeling of Serotonin Receptors Byd-[3H]Lysergic Acid
    Proc. Nati. Acad. Sci. USA Vol. 75, No. 12, pp. 5783-5787, December 1978 Biochemistry Selective labeling of serotonin receptors by d-[3H]lysergic acid diethylamide in calf caudate (ergots/hallucinogens/tryptamines/norepinephrine/dopamine) PATRICIA M. WHITAKER AND PHILIP SEEMAN* Department of Pharmacology, University of Toronto, Toronto, Canada M5S 1A8 Communicated by Philip Siekevltz, August 18,1978 ABSTRACT Since it was known that d-lysergic acid di- The objective in this present study was to improve the se- ethylamide (LSD) affected catecholaminergic as well as sero- lectivity of [3H]LSD for serotonin receptors, concomitantly toninergic neurons, the objective in this study was to enhance using other drugs to block a-adrenergic and dopamine receptors the selectivity of [3HJISD binding to serotonin receptors in vitro by using crude homogenates of calf caudate. In the presence of (cf. refs. 36-38). We then compared the potencies of various a combination of 50 nM each of phentolamine (adde to pre- drugs on this selective [3H]LSD binding and compared these clude the binding of [3HJLSD to a-adrenoceptors), apmo ie, data to those for the high-affinity binding of [3H]serotonin and spiperone (added to preclude the binding of [3H[LSD to (39). dopamine receptors), it was found by Scatchard analysis that the total number of 3H sites went down to 300 fmol/mg, compared to 1100 fmol/mg in the absence of the catechol- METHODS amine-blocking drugs. The IC50 values (concentrations to inhibit Preparation of Membranes. Calf brains were obtained fresh binding by 50%) for various drugs were tested on the binding of [3HLSD in the presence of 50 nM each of apomorphine (A), from the Canada Packers Hunisett plant (Toronto).
    [Show full text]
  • Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanismss
    Supplemental Material can be found at: /content/suppl/2020/12/18/73.1.202.DC1.html 1521-0081/73/1/202–277$35.00 https://doi.org/10.1124/pharmrev.120.000056 PHARMACOLOGICAL REVIEWS Pharmacol Rev 73:202–277, January 2021 Copyright © 2020 by The Author(s) This is an open access article distributed under the CC BY-NC Attribution 4.0 International license. ASSOCIATE EDITOR: MICHAEL NADER Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanismss Antonio Inserra, Danilo De Gregorio, and Gabriella Gobbi Neurobiological Psychiatry Unit, Department of Psychiatry, McGill University, Montreal, Quebec, Canada Abstract ...................................................................................205 Significance Statement. ..................................................................205 I. Introduction . ..............................................................................205 A. Review Outline ........................................................................205 B. Psychiatric Disorders and the Need for Novel Pharmacotherapies .......................206 C. Psychedelic Compounds as Novel Therapeutics in Psychiatry: Overview and Comparison with Current Available Treatments . .....................................206 D. Classical or Serotonergic Psychedelics versus Nonclassical Psychedelics: Definition ......208 Downloaded from E. Dissociative Anesthetics................................................................209 F. Empathogens-Entactogens . ............................................................209
    [Show full text]
  • Guideline- Management of Migraine and Cluster Headache
    Hull & East Riding Prescribing Committee Guideline- Management of Migraine and Cluster Headache 1. BACKGROUND Headache is a common neurological condition which accounts for 4.4% of primary care consultations and 30% of neurology appointments. Primary headache disorders include migraine, tension-type and cluster headache. Twice as many women as men are affected by headache disorder. This is thought to be due to changes in hormone levels during the menstrual cycle, which can be more pronounced at puberty and menopause. Recommendations within this guideline are based on best evidence and national/international guidelines. They are followed by consultants and specialist nurses working within the neurology department. Some recommendations may be for medicines prescribed outside their product license i.e. off label. It is noted in the guideline when the medicine is off label and relevant guidelines should be followed when prescribing medicines off label. A number of British Association for the Study of Headache (BASH) leaflets have been linked in this guidance; these can be given to patients and cover the off license use of medicines and information about duration of prophylactic treatments. The colours on the drug names in this guidance refer to the classification in the joint formulary i.e. Red – specialist prescriber only Amber – prescribed in accordance with approved shared care framework Blue - Guideline Led prescribed on advice of specialist or in line with national / local guideline Green – other items listed on formulary suitable for initiation and prescribing by any prescriber If printed in black and white please refer to joint formulary for classification of medicines. Migraine Migraine is often underdiagnosed, misdiagnosed and undertreated.
    [Show full text]
  • Migraine Headache Prophylaxis Hien Ha, Pharmd, and Annika Gonzalez, MD, Christus Santa Rosa Family Medicine Residency Program, San Antonio, Texas
    Migraine Headache Prophylaxis Hien Ha, PharmD, and Annika Gonzalez, MD, Christus Santa Rosa Family Medicine Residency Program, San Antonio, Texas Migraines impose significant health and financial burdens. Approximately 38% of patients with episodic migraines would benefit from preventive therapy, but less than 13% take prophylactic medications. Preventive medication therapy reduces migraine frequency, severity, and headache-related distress. Preventive therapy may also improve quality of life and prevent the progression to chronic migraines. Some indications for preventive therapy include four or more headaches a month, eight or more headache days a month, debilitating headaches, and medication- overuse headaches. Identifying and managing environmental, dietary, and behavioral triggers are useful strategies for preventing migraines. First-line med- ications established as effective based on clinical evidence include divalproex, topiramate, metoprolol, propranolol, and timolol. Medications such as ami- triptyline, venlafaxine, atenolol, and nadolol are probably effective but should be second-line therapy. There is limited evidence for nebivolol, bisoprolol, pindolol, carbamazepine, gabapentin, fluoxetine, nicardipine, verapamil, nimodipine, nifedipine, lisinopril, and candesartan. Acebutolol, oxcarbazepine, lamotrigine, and telmisartan are ineffective. Newer agents target calcitonin gene-related peptide pain transmission in the migraine pain pathway and have recently received approval from the U.S. Food and Drug Administration; ​​​how- ever, more studies of long-term effectiveness and adverse effects are needed. The complementary treatments petasites, feverfew, magnesium, and riboflavin are probably effective. Nonpharmacologic therapies such as relaxation training, thermal biofeedback combined with relaxation training, electromyographic feedback, and cognitive behavior therapy also have good evidence to support their use in migraine prevention. (Am Fam Physician. 2019; 99(1):17-24.
    [Show full text]
  • DBL™ Promethazine Hydrochloride Injection BP
    DBL™ Promethazine Hydrochloride Injection BP 1. NAME OF THE MEDICINE Promethazine hydrochloride 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Each mL of the solution contains 25.0 mg promethazine hydrochloride, 0.10 mg disodium edetate, 1.30 microlitre glacial acetic acid, 27.2 mg sodium acetate and 1.32 mg sodium metabisulfite in water for injections. Excipient(s) with known effect Sodium metabisulfite For the full list of excipients, see section 6.1 List of Excipients. 3. PHARMACEUTICAL FORM Solution for injection. DBL™ Promethazine Hydrochloride Injection BP is a clear, colourless solution of pH 5.0 to 6.0. 4. CLINICAL PARTICULARS 4.1 Therapeutic Indications DBL™ Promethazine Hydrochloride Injection BP is indicated for the following conditions: Treatment of allergic reactions such as: uncomplicated allergic conditions of the immediate type, e.g., pruritus, urticaria and angioedema, when oral therapy is impossible or contraindicated. Treatment and prevention of vomiting including: motion sickness; drug induced nausea; prevention and control of nausea and vomiting associated with certain types of anaesthesia and surgery, such as procedures with a high incidence of post-operative vomiting (e.g., gynaecological surgery, strabismus or middle ear surgery, and electroconvulsive therapy); in patients with a past history of motion sickness or post- operative vomiting; and in patients in whom avoidance of vomiting is crucial (e.g., neurosurgery and eye surgery). Page 1 of 10 Promethazine has sedative effects and it is also used in: pre-operative, post-operative and obstetric (during labour) sedation. 4.2 Dose and Method of Administration Dosage Allergic conditions Adults: 25 mg to 50 mg by deep intramuscular injection or slow intravenous injection; may be repeated within two hours if necessary.
    [Show full text]
  • Tcas Versus Placebo - New Studies in the Guideline Update
    TCAs versus placebo - new studies in the guideline update Comparisons Included in this Clinical Question Amitriptyline vs placebo Clomipramine vs placebo Dosulepin (dothiepin) vs placebo AMSTERDAM2003A LARSEN1989 FERGUSON1994B BAKISH1992B PECKNOLD1976B ITIL1993 BAKISH1992C RAMPELLO1991 MINDHAM1991 BREMNER1995 THOMPSON2001B CLAGHORN1983 CLAGHORN1983B FEIGHNER1979 GELENBERG1990 GEORGOTAS1982A GOLDBERG1980 HICKS1988 HOLLYMAN1988 HORMAZABAL1985 HOSCHL1989 KLIESER1988 LAAKMAN1995 LAPIERRE1991 LYDIARD1997 MYNORSWALLIS1995 MYNORSWALLIS1997 REIMHERR1990 RICKELS1982D RICKELS1985 RICKELS1991 ROFFMAN1982 ROWAN1982 SMITH1990 SPRING1992 STASSEN1993 WILCOX1994 16 Imipramine vs placebo BARGESCHAAPVELD2002 BEASLEY1991B BOYER1996A BYERLEY1988 CASSANO1986 CASSANO1996 CLAGHORN1996A COHN1984 COHN1985 COHN1990A COHN1992 COHN1996 DOMINGUEZ1981 DOMINGUEZ1985 DUNBAR1991 ELKIN1989 ENTSUAH1994 ESCOBAR1980 FABRE1980 FABRE1992 FABRE1996 FEIGER1996A FEIGHNER1980 FEIGHNER1982 FEIGHNER1983A FEIGHNER1983B FEIGHNER1989 FEIGHNER1989A FEIGHNER1989B FEIGHNER1989C FEIGHNER1992B FEIGHNER1993 FONTAINE1994 GELENBERG2002 GERNER1980B HAYES1983 ITIL1983A KASPER1995B KELLAMS1979 LAIRD1993 LAPIERRE1987 LECRUBIER1997B LIPMAN1986 LYDIARD1989 MARCH1990 17 MARKOWITZ1985 MENDELS1986 MERIDETH1983 Nortriptyline vs placebo NANDI1976 GEORGOTAS1986A NORTON1984 KATZ1990 PEDERSEN2002 NAIR1995 PESELOW1989 WHITE1984A PESELOW1989B PHILIPP1999 QUITKIN1989 RICKELS1981 RICKELS1982A RICKELS1987 SCHWEIZER1994 SCHWEIZER1998 SHRIVASTAVA1992 SILVERSTONE1994 SMALL1981 UCHA1990 VERSIANI1989 VERSIANI1990
    [Show full text]
  • Headaches Return Frequently Enough to Justify Resuming Intractable Headache
    Interference with school work justifies treatment in childhood. of sedation and analgesics in hospital. Steroids can be given, Propranolol was the first drug shown to reduce the but their use has not been closely scrutinised. frequency ofmigraine attacks,'9 and it is effective in 60-80% of CHRIS CLOUGH patients.' How it works is unknown; g blockade alone is Consultant Neurologist, unlikely to be responsible. Propranolol lacks intrinsic sympa- Brook General Hospital, London SE8 4LW thetic activity,20 a property shared with atenolol, metroprolol, BMJ: first published as 10.1136/bmj.299.6692.142 on 15 July 1989. Downloaded from and timoloF'-0 blockers cannot be used in obstructive 1 Wilkinson M. Iigraine-the treatment of acute attack. Scott MedJ 1985;4:258-62. airways disease or heart block, and their use is commonly 2 Steiner TJ, Guha P, Capildeo R, Rose FC. Migraine in patients attending a migraine clinic. Headache 1980;20:190-5. accompanied by side effects, of which lethargy is the most 3 Perkin JE, Hartjc J. Diet and migraine: A review of the literature.JA7m DietAssoc 1983;83:459-63. prominent. 4 Moffett A, Swash MNS, Scott DF. Effect of tvramine in migraine: a double blind study. J Neurol Neurosurg Psvchiatrv 1972;35:496-9. Propranolol 40 mg twice daily should be prescribed initially, 5 Rao NS, Pearce JMS. Hypothalamic-pituitary-adrenal axis studies in migraine with special reference to insulin sensitivity. Brain 1971;94(part II):289-98. increasing ifnecessary to 80 mg thrice daily. Long acting once 6 Egger J, Wilson J, Carter CM\, 'I'urner MIW, Soothill JF.
    [Show full text]
  • Propranolol 10Mg, 40Mg, 80Mg and 160Mg Tablets
    • worsening of your blood circulation, if you 6 Contents of the pack and other already suffer from poor circulation information • worsening of breathing difficulties, if you have or What Propranolol tablets contain have had asthma • the active substance (the ingredient that makes • hair loss, skin rash, including worsening of the tablets work) is propranolol hydrochloride. Package leaflet: Information for the patient psoriasis, purple spots on the skin (purpura) Each tablet contains either 10mg, 40mg, 80mg or 160mg of the active substance. Propranolol 10mg, 40mg, 80mg Very rare (may affect up to 1 in 10,000 • the other ingredients are lactose, magnesium people) stearate, maize starch, stearic acid, hypromellose and 160mg tablets • severe muscle weakness (myasthenia gravis) (E464). • there may be changes to some of the cells or • the coating contains polysorbate, carmoisine other parts of your blood. It is possible that your (E122), titanium dioxide (E171), iron oxide red Read all of this leaflet carefully before • prevention of migraine doctor may occasionally take blood samples to (E172), hypromellose (E464). you start taking this medicine because it • essential tremor, anxiety check whether propranolol has had any effect contains important information for you. • certain thyroid conditions (such as on your blood. What Propranolol tablets look like and • Keep this leaflet. You may need to read it thyrotoxicosis, which is caused by an contents of the pack again. overactive thyroid gland) Not known (frequency cannot be Propranolol tablets 10mg are pink, circular, • If you have any further questions, ask your • hypertrophic cardiomyopathy (thickened estimated from the available data): biconvex film-coated tablets impressed “C” on doctor or pharmacist.
    [Show full text]
  • Effects of Antidepressant Treatment on Inhibitory Avoidance Behavior and Amygdaloid ␤-Adrenoceptors in Rats Lynette C
    Effects of Antidepressant Treatment on Inhibitory Avoidance Behavior and Amygdaloid b-Adrenoceptors in Rats Lynette C. Daws, Ph.D., Ray Lopez, Ph.D., and Alan Frazer, Ph.D. Chronic treatment of rats with a variety of antidepressants showed a marked deficit in retention. This effect was also b results in the down-regulation of 1-adrenoceptors in the observed after acute administration of these drugs, although b amygdaloid nuclei. The present study sought to determine if they did not down-regulate amygdaloid 1-adrenoceptors at this specific neurochemical effect caused an alteration in this time. It seems that the ability of these antidepressants to inhibitory avoidance conditioning, a behavior considered to potentiate the amnesic effect of scopolamine is unrelated to b b be mediated by -adrenoceptors in the amygdala. Rats their effect on 1-adrenoceptor number in the amygdala and b treated chronically with either desipramine (DMI) or that the extent of antidepressant-induced amygdaloid 1- b phenelzine (PHEN), which down-regulate 1-adrenoceptors adrenoceptor down-regulation is not sufficient, by itself, to in the amygdala, or fluoxetine (FLUOX), which does not do cause a deficit in an inhibitory avoidance task. this, did not exhibit a deficit in the retention of the [Neuropsychopharmacology 19:300–313, 1998] inhibitory avoidance task. However, when scopolamine was © 1998 American College of Neuropsychopharmacology. given prior to acquisition of the task in a dose that, by itself, Published by Elsevier Science Inc. did not affect retention, DMI- and PHEN-treated rats KEY WORDS: Inhibitory avoidance; Desipramine; ous reports emphasizing the putative role of the b Phenelzine; Fluoxetine; 1-Adrenoceptors; Amygdala amygdala in mediating the behavioral actions of antide- pressants (Horovitz 1966; Gorka et al.
    [Show full text]
  • Triptolol Is Once a Day at Bedtime
    1. Generic Name Amitriptyline Hydrochloride + Propranolol Hydrochloride 2. Qualitative and Quantitative Composition Amitriptyline Hydrochloride IP 10mg Propranolol Hydrochloride IP 40mg 3. Dosage form and strength Oral tablets are available in the strength of Amitriptyline 10mg, Propranolol 40mg 4. Clinical particulars 4.1 Therapeutic indication Migraine with co-morbid conditions like Insomnia, Neuralgic Pain, Hypertension, Anxiety 4.2 Posology and method of administration Recommended oral dose of Triptolol is once a day at bedtime. 4.3 Contraindication The use of Triptolol Tablet is contraindicated in patients with: • Known hypersensitivity to any ingredient in this product. • On prescription of MAO inhibiting compound. • Severe hepatic dysfunction. • history of urinary retention – BPH • cardiogenic Shock, sinus Bradycardia and greater than first degree block, bronchial Asthma 4.4 Special warnings and precautions for use • Triptolol Tablet should be used with caution in patients with renal or hepatic dysfunction and cardiovascular problems. • Caution is advised in untreated angle-closure glaucoma, phaeochromocytoma, and hyperthyroidism. • Avoid consuming alcohol when taking the Triptolol as it may cause excessive drowsiness. 4.5 Drug interactions • Amitriptyline Most common (but not the only) medications used that have the potential for major drug interactions when combined with amitriptyline are duloxetine, citalopram, fluoxetine, topiramate, tramadol, sertraline, cyclobenzaprine and trazodone Most common (but not the only) medications
    [Show full text]