Ajmaline: An alkaloid found in the root of RAUWOLFIA SERPENTINA, among other plant sources. It is a class Ia antiarrhythmic agent that apparently acts by changing the shape and threshold of cardiac action potentials.Rauwolfia: A plant genus of the APOCYNACEAE or dogbane family. Alkaloids from plants in this genus have been used as tranquilizers and antihypertensive agents. RESERPINE is derived from R. serpentina.Brugada Syndrome: An autosomal dominant defect of cardiac conduction that is characterized by an abnormal ST-segment in leads V1-V3 on the ELECTROCARDIOGRAM resembling a right BUNDLE-BRANCH BLOCK; high risk of VENTRICULAR TACHYCARDIA; or VENTRICULAR FIBRILLATION; SYNCOPAL EPISODE; and possible sudden death. This syndrome is linked to mutations of gene encoding the cardiac SODIUM CHANNEL alpha subunit.Secologanin Tryptamine Alkaloids: Compounds formed by condensation of secologanin with tryptamine resulting in a tetrahydro-beta-carboline which is processed further to a number of bioactive compounds. These are especially found in plants of the APOCYNACEAE; LOGANIACEAE; and RUBIACEAE families.Anti-Arrhythmia Agents: Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.Electrocardiography: Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.Bundle-Branch Block: A form of heart block in which the electrical stimulation of HEART VENTRICLES is interrupted at either one of the branches of BUNDLE OF HIS thus preventing the simultaneous depolarization of the two ventricles.Fonofos: An organothiophosphorus cholinesterase inhibitor that is used as an insecticide.Chemical Industry: The aggregate enterprise of manufacturing and technically producing chemicals. (From Random House Unabridged Dictionary, 2d ed)Environmental Pollutants: Substances or energies, for example heat or light, which when introduced into the air, water, or land threaten life or health of individuals or ECOSYSTEMS.Occupational Exposure: The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation.Directories as Topic: Lists of persons or organizations, systematically arranged, usually in alphabetic or classed order, giving address, affiliations, etc., for individuals, and giving address, officers, functions, and similar data for organizations. (ALA Glossary of Library and Information Science, 1983)Phytochemicals: A broad range of biologically active compounds which occur naturally in plants having important medicinal and nutritional properties.Manufactured Materials: Substances and materials manufactured for use in various technologies and industries and for domestic use.Industry: Any enterprise centered on the processing, assembly, production, or marketing of a line of products, services, commodities, or merchandise, in a particular field often named after its principal product. Examples include the automobile, fishing, music, publishing, insurance, and textile industries.Industrial Oils: Oils which are used in industrial or commercial applications.Organic Chemicals: A broad class of substances containing carbon and its derivatives. Many of these chemicals will frequently contain hydrogen with or without oxygen, nitrogen, sulfur, phosphorus, and other elements. They exist in either carbon chain or carbon ring form.Particle Size: Relating to the size of solids.Volatile Organic Compounds: Organic compounds that have a relatively high VAPOR PRESSURE at room temperature.Chemistry, Organic: The study of the structure, preparation, properties, and reactions of carbon compounds. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Water Pollutants, Chemical: Chemical compounds which pollute the water of rivers, streams, lakes, the sea, reservoirs, or other bodies of water.Cosmic Dust: Finely divided solid matter with particle sizes smaller than a micrometeorite, thus with diameters much smaller than a millimeter, moving in interplanetary space. (NASA Thesaurus, 1994)Meteoroids: Any solid objects moving in interplanetary space that are smaller than a planet or asteroid but larger than a molecule. Meteorites are any meteoroid that has fallen to a planetary surface. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Domperidone: A specific blocker of dopamine receptors. It speeds gastrointestinal peristalsis, causes prolactin release, and is used as antiemetic and tool in the study of dopaminergic mechanisms.Galactogogues: Substances that induce LACTATION.Gastrointestinal Motility: The motor activity of the GASTROINTESTINAL TRACT.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Gastroesophageal Reflux: Retrograde flow of gastric juice (GASTRIC ACID) and/or duodenal contents (BILE ACIDS; PANCREATIC JUICE) into the distal ESOPHAGUS, commonly due to incompetence of the LOWER ESOPHAGEAL SPHINCTER.Suppositories: Medicated dosage forms that are designed to be inserted into the rectal, vaginal, or urethral orifice of the body for absorption. Generally, the active ingredients are packaged in dosage forms containing fatty bases such as cocoa butter, hydrogenated oil, or glycerogelatin that are solid at room temperature but melt or dissolve at body temperature.Gastrointestinal Diseases: Diseases in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.Alcohols: Alkyl compounds containing a hydroxyl group. They are classified according to relation of the carbon atom: primary alcohols, R-CH2OH; secondary alcohols, R2-CHOH; tertiary alcohols, R3-COH. (From Grant & Hackh's Chemical Dictionary, 5th ed)Alcohol Drinking: Behaviors associated with the ingesting of alcoholic beverages, including social drinking.Alcohol Dehydrogenase: A zinc-containing enzyme which oxidizes primary and secondary alcohols or hemiacetals in the presence of NAD. In alcoholic fermentation, it catalyzes the final step of reducing an aldehyde to an alcohol in the presence of NADH and hydrogen.KetonesAlcohol Oxidoreductases: A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. They are further classified according to the acceptor which can be NAD+ or NADP+ (subclass 1.1.1), cytochrome (1.1.2), oxygen (1.1.3), quinone (1.1.5), or another acceptor (1.1.99).Butanols: Isomeric forms and derivatives of butanol (C4H9OH).PropaneDrug Information Services: Services providing pharmaceutic and therapeutic drug information and consultation.Pamphlets: Printed publications usually having a format with no binding and no cover and having fewer than some set number of pages. They are often devoted to a single subject.Drug Labeling: Use of written, printed, or graphic materials upon or accompanying a drug container or wrapper. It includes contents, indications, effects, dosages, routes, methods, frequency and duration of administration, warnings, hazards, contraindications, side effects, precautions, and other relevant information.Patient Education as Topic: The teaching or training of patients concerning their own health needs.Formularies as Topic: Works about lists of drugs or collections of recipes, formulas, and prescriptions for the compounding of medicinal preparations. Formularies differ from PHARMACOPOEIAS in that they are less complete, lacking full descriptions of the drugs, their formulations, analytic composition, chemical properties, etc. In hospitals, formularies list all drugs commonly stocked in the hospital pharmacy.Drug Industry: That segment of commercial enterprise devoted to the design, development, and manufacture of chemical products for use in the diagnosis and treatment of disease, disability, or other dysfunction, or to improve function.Medical Records Systems, Computerized: Computer-based systems for input, storage, display, retrieval, and printing of information contained in a patient's medical record.Facial Muscles: Muscles of facial expression or mimetic muscles that include the numerous muscles supplied by the facial nerve that are attached to and move the skin of the face. (From Stedman, 25th ed)Diplopia: A visual symptom in which a single object is perceived by the visual cortex as two objects rather than one. Disorders associated with this condition include REFRACTIVE ERRORS; STRABISMUS; OCULOMOTOR NERVE DISEASES; TROCHLEAR NERVE DISEASES; ABDUCENS NERVE DISEASES; and diseases of the BRAIN STEM and OCCIPITAL LOBE.Migraine Disorders: A class of disabling primary headache disorders, characterized by recurrent unilateral pulsatile headaches. The two major subtypes are common migraine (without aura) and classic migraine (with aura or neurological symptoms). (International Classification of Headache Disorders, 2nd ed. Cephalalgia 2004: suppl 1)Tryptamines: Decarboxylated monoamine derivatives of TRYPTOPHAN.Chest Pain: Pressure, burning, or numbness in the chest.Jaw: Bony structure of the mouth that holds the teeth. It consists of the MANDIBLE and the MAXILLA.Universal Precautions: Prudent standard preventive measures to be taken by professional and other health personnel in contact with persons afflicted with a communicable disease, to avoid contracting the disease by contagion or infection. Precautions are especially applicable in the diagnosis and care of AIDS patients.
ATP- and glutathione-dependent transport of chemotherapeutic drugs by the multidrug resistance protein MRP1. (1/40)
The present study was performed to investigate the ability of the multidrug resistance protein (MRPI) to transport different cationic substrates in comparison with MDR1-P-glycoprotein (MDR1). Transport studies were performed with isolated membrane vesicles from in vitro selected multidrug resistant cell lines overexpressing MDR1 (A2780AD) or MRP1 (GLC4/Adr) and a MRP1-transfected cell line (S1(MRP)). As substrates we used 3H-labelled derivatives of the hydrophilic monoquaternary cation N-(4',4'-azo-in-pentyl)-21-deoxy-ajmalinium (APDA), the basic drug vincristine and the more hydrophobic basic drug daunorubicin. All three are known MDR1-substrates. MRP1 did not mediate transport of these substrates per se. In the presence of reduced glutathione (GSH), there was an ATP-dependent uptake of vincristine and daunorubicin, but not of APDA, into GLC4/Adr and S1(MRP) membrane vesicles which could be inhibited by the MRP1-inhibitor MK571. ATP- and GSH-dependent transport of daunorubicin and vincristine into GLC4/Adr membrane vesicles was inhibited by the MRP1-specific monoclonal antibody QCRL-3. MRP1-mediated daunorubicin transport rates were dependent on the concentration of GSH and were maximal at concentrations > or = 10 mM. The apparent KM value for GSH was 2.7 mM. Transport of daunorubicin in the presence of 10 mM GSH was inhibited by MK571 with an IC50 of 0.4 microM. In conclusion, these results demonstrate that MRP1 transports vincristine and daunorubicin in an ATP- and GSH-dependent manner. APDA is not a substrate for MRP1. (+info)Sudden death in patients and relatives with the syndrome of right bundle branch block, ST segment elevation in the precordial leads V(1)to V(3)and sudden death. (2/40)
BACKGROUND: The syndrome with an electrocardiographic pattern of right bundle branch block, ST segment elevation in leads V(1)to V(3)and sudden death is genetically determined and caused by mutations in the cardiac sodium channel. The inheritance of the disease is autosomal dominant. Sudden death may, however, occur from a variety of causes in relatives and patients with this syndrome. PATIENTS AND METHODS: Twenty-five Flemish families with this syndrome with a total of 334 members were studied. Affected members were recognized by means of a typical electrocardiogram either occurring spontaneously or after the intravenous administration of antiarrhythmic drugs. Sudden deaths in these families were classified as related or not to the syndrome by analysis of the data at the time of the event, mode of inheritance of the disease, and data provided by survivors. Results Of the 25 families with the syndrome, 18 were symptomatic (at least one sudden death related to the syndrome) and seven were asymptomatic (no sudden deaths related to the syndrome). In total, there were 42 sudden cardiac deaths (12% incidence). Twenty-four sudden deaths were related to the syndrome and all occurred in symptomatic families. Eighteen sudden deaths (43% of total sudden deaths) were not related to the syndrome (nine cases) or were of unclear cause (nine cases). Three of them occurred in two asymptomatic families and the remaining 15 in five symptomatic families. Twenty-four of the 50 affected members (47%) suffered (aborted) sudden death and 18 of the 284 unaffected members (6%). This difference in the incidence of sudden death was statistically significant (P<0.0001). Patients with (aborted) sudden death caused by the syndrome were younger than patients with sudden death of other or unclear causes (38+/-4 years vs 59+/-3 years respectively, P=0.0003). CONCLUSIONS: In families at high risk of sudden death because of genetically determined diseases, the main cause of sudden death remains the disease. However, almost the half of sudden deaths are caused by unrelated diseases or are of unclear cause. Accurate classification of the causes of sudden death is mandatory for appropriate analysis of the causes of death when designing preventive treatments. (+info)Body surface potential mapping in patients with Brugada syndrome: right precordial ST segment variations and reverse changes in left precordial leads. (3/40)
OBJECTIVE: The aim of this study was to perform quantitative signal analysis of high-resolution body surface potential mapping (BSPM) recordings to assess its usefulness for the electrocardiographic characterization of patients with Brugada syndrome. The diagnostic value of the QRS integral and of the gradient of the ST segment have not been elucidated in Brugada syndrome. METHODS: In 27 subjects (16 with Brugada syndrome and 11 healthy subjects), 120-lead BSPMs were recorded at baseline and after pharmacological provocation with intravenous administration of ajmaline (1 mg/kg). The recordings were analyzed for two regions outside the positions of the standard ECG leads: the right precordial leads (RPL) on the second and third intercostal space (high RPL) and the left precordial leads (LPL) between the fifth and seventh intercostal space (low LPL). RESULTS: At baseline, in high RPL regions, patients with Brugada syndrome showed more positive QRS integrals (-5+/-8 vs. -16+/-8 mV ms) and a steeper negative ST segment gradient (-0.62+/-0.41 vs. -0.29+/-0.40 mV/s) compared to healthy subjects, P<0.001. In contrast, in low LPL regions, reduced QRS integrals and positive ST segment gradients were observed. These ECG signs were even more pronounced after intravenous ajmaline and showed a better discrimination for patients with Brugada syndrome than differences in RPL or LPL during baseline, respectively. CONCLUSIONS: In the left precordial leads, patients with Brugada syndrome showed ECG changes which were reversed in relation to the ECG changes observed in right precordial leads. BSPM measurement is a useful tool to improve the understanding of the electrocardiographic changes in the Brugada syndrome. (+info)Antiarrhythmic effect of aprindine on several types of ventricular arrhythmias. (4/40)
The antiarrhythmic effect of aprindine was compared with those of lidocaine and propranolol on several ventricular arrhythmias-epinephrine arrhythmias in cats, ouabain arrhythmias in cats and guinea pigs, ischemic ventricular arrhythmias in coronary-ligated Beagle dogs. Antiarrhythmic effects of aprindine and lidocaine were observed both in ouagain and ischemic arrhythmias, but not in epinephrine arrhythmias. While propranolol had a strong antiarrhythmic effect against epinephrine and ouabain arrhythmias, it did not increase sinus beats in ischemic arrhythmias. Marked anti-arrhythmic effects of aprindine in ischemic arrhythmias were observed in dogs using either single intravenous administration (4 mg/kg) or intravenous infusion (200 mug/kg/min, 2 mg/kg). Antiarrhythmic activity of aprindine is considered to be about twice as strong as that of lidocaine, but lidocaine is less toxic in experimental animals. (+info)The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol. (5/40)
AIMS: The diagnostic ECG pattern in Brugada syndrome (BS) can transiently normalize and may be unmasked by sodium channel blockers such as ajmaline. Proarrhythmic effects of the drug have been well documented in the literature. A detailed protocol for the ajmaline challenge in Brugada syndrome has not yet been described. Therefore, we prospectively studied the risks of a standardized ajmaline test. METHODS AND RESULTS: During a period of 60 months, 158 patients underwent the ajmaline test in our institution. Ajmaline was given intravenously in fractions (10mg every two minutes) up to a target dose of 1mg/kg. In 37 patients (23%) the typical coved-type ECG pattern of BS was unmasked. During the test, symptomatic VT appeared in 2 patients (1.3%). In all other patients, the drug challenge did not induce VT if the target dose, QRS prolongation >30%, presence/appearance of the typical ECG, or the occurrence of premature ventricular ectopy were considered as end points of the test. A positive response to ajmaline was induced in 2 of 94 patients (2%) with a normal baseline ECG, who underwent evaluation solely for syncope of unknown origin. CONCLUSION: The ajmaline challenge using a protocol with fractionated drug administration is a safe method to diagnose BS. Because of the potential induction of VT, it should be performed under continuous medical surveillance with advanced life-support facilities. Due to the prognostic importance all patients with aborted sudden death or unexplained syncope without demonstrable structural heart disease and family members of affected individuals should presently undergo drug testing for unmasking BS. (+info)Unusual response to the ajmaline test in a patient with Brugada syndrome. (6/40)
We present a Brugada syndrome patient who suffered an aborted sudden death. The ajmaline test (1 mg/kg body weight) induced accentuated alternans ST-segment elevation in V1-V2 without ventricular arrhythmias. It could represent silent ischaemia not detected before, failure of myocardial regions to repolarize in alternate beats due to transmural dispersion of conduction and refractoriness in the right ventricular outflow tract or a rate dependent sodium channel block by ajmaline. We need more studies to know whether this electrocardiographic sign is a risk factor for life-threatening ventricular arrhythmias in Brugada syndrome patients. (+info)Value of electrocardiographic parameters and ajmaline test in the diagnosis of Brugada syndrome caused by SCN5A mutations. (7/40)
BACKGROUND: The Brugada syndrome is an arrhythmogenic disease caused in part by mutations in the cardiac sodium channel gene, SCN5A. The electrocardiographic pattern characteristic of the syndrome is dynamic and is often absent in affected individuals. Sodium channel blockers are effective in unmasking carriers of the disease. However, the value of the test remains controversial. METHODS AND RESULTS: We studied 147 individuals representing 4 large families with SCN5A mutations. Of these, 104 were determined to be at possible risk for Brugada syndrome and underwent both electrocardiographic and genetic evaluation. Twenty-four individuals displayed an ECG diagnostic of Brugada syndrome at baseline. Of the remaining, 71 received intravenous ajmaline. Of the 35 genetic carriers who received ajmaline, 28 had a positive test and 7 a negative ajmaline test. The sensitivity, specificity, and positive and negative predictive values of the drug challenge were 80% (28:35), 94.4% (34:36), 93.3% (28:30), and 82.9% (34:41), respectively. Penetrance of the disease phenotype increased from 32.7% to 78.6% with the use of sodium channel blockers. In the absence of ST-segment elevation under baseline conditions, a prolonged P-R interval, but not incomplete right bundle-branch block or early repolarization patterns, indicates a high probability of an SCN5A mutation carrier. CONCLUSIONS: In families with Brugada syndrome, the data suggest that ajmaline testing is valuable in the diagnosis of SCN5A carriers. In the absence of ST-segment elevation at baseline, family members with first-degree atrioventricular block should be suspected of carrying the mutation. An ajmaline test is often the key to making the proper diagnosis in these patients. (+info)Crystal structure of vinorine synthase, the first representative of the BAHD superfamily. (8/40)
Vinorine synthase is an acetyltransferase that occupies a central role in the biosynthesis of the antiarrhythmic monoterpenoid indole alkaloid ajmaline in the plant Rauvolfia. Vinorine synthase belongs to the benzylalcohol acetyl-, anthocyanin-O-hydroxy-cinnamoyl-, anthranilate-N-hydroxy-cinnamoyl/benzoyl-, deacetylvindoline acetyltransferase (BAHD) enzyme superfamily, members of which are involved in the biosynthesis of several important drugs, such as morphine, Taxol, or vindoline, a precursor of the anti-cancer drugs vincaleucoblastine and vincristine. The x-ray structure of vinorine synthase is described at 2.6-angstrom resolution. Despite low sequence identity, the two-domain structure of vinorine synthase shows surprising similarity with structures of several CoA-dependent acyltransferases such as dihydrolipoyl transacetylase, polyketide-associated protein A5, and carnitine acetyltransferase. All conserved residues typical for the BAHD family are found in domain 1. His160 of the HXXXD motif functions as a general base during catalysis. It is located in the center of the reaction channel at the interface of both domains and is accessible from both sides. The channel runs through the entire molecule, allowing the substrate and co-substrate to bind independently. Asp164 points away from the catalytic site and seems to be of structural rather than catalytic importance. Surprisingly, the DFGWG motif, which is indispensable for the catalyzed reaction and unique to the BAHD family, is located far away from the active site and seems to play only a structural role. Vinorine synthase represents the first solved protein structure of the BAHD superfamily. (+info)Part I. Ajmaline series. Journal of the Indian Chemical Society. 9. p. 539. Siddiqui, S. and Siddiqui, R.H. (1935). The ... Ajmaline series. Journal of the Indian Chemical Society. 12. p. 37. Siddiqui, S. (1942). A note on isolation of three new ... He named the newly discovered chemical compound as Ajmaline, after his mentor Hakim Ajmal Khan who was one of the illustrious ... "Value of Electrocardiographic Parameters and Ajmaline Test in the Diagnosis of Brugada Syndrome Caused by SCN5A Mutations". ...
... is a member of the sodium channel blocking class of antiepileptic drugs.[60] This may suppress the release of glutamate and aspartate, two of the dominant excitatory neurotransmitters in the CNS.[61] It is generally accepted to be a member of the sodium channel blocking class of antiepileptic drugs,[62] but it could have additional actions since it has a broader spectrum of action than other sodium channel antiepileptic drugs such as phenytoin and is effective in the treatment of the depressed phase of bipolar disorder, whereas other sodium channel blocking antiepileptic drugs are not, possibly on account of its sigma receptor activity. In addition, lamotrigine shares few side-effects with other, unrelated anticonvulsants known to inhibit sodium channels, which further emphasises its unique properties.[63] It is a triazine derivate that inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membranes. It also blocks L-, N-, and P-type calcium channels and ...
The hormone prolactin stimulates lactation (production of breast milk). Dopamine, released by the hypothalamus stops the release of prolactin from the pituitary gland. Domperidone, by acting as an anti-dopaminergic agent, results in increased prolactin secretion, and thus promotes lactation (that is, it is a galactogogue). In some nations, including Australia, domperidone is used off-label, based on uncertain and anecdotal evidence of its usefulness, as a therapy for mothers who are having difficulty breastfeeding.[24][25] In the United States, domperidone is not approved for this or any other use.[26][27] A study called the EMPOWER trial was designed to assess the effectiveness and safety of domperidone in assisting mothers of preterm babies to supply breast milk for their infants.[28] The study randomized 90 mothers of preterm babies to receive either domperidone 10 mg orally three times daily for 28 days (Group A) or placebo 10 mg orally three times daily for 14 days followed by domperidone ...
... (DHP) is a molecule based upon pyridine, and the parent of a class of molecules that have been semi-saturated with two substituents replacing one double bond. They are particularly well known in pharmacology as L-type calcium channel blockers, used in the treatment of hypertension. Compared with certain other L-type calcium channel blockers (for example those of the phenylalkylamine class such as verapamil) that have significant action at the heart, they are relatively vascular selective in their mechanism of action in lowering blood pressure. ...
InChI=1S/C20H27N5O5S/c1-15-14-18(23-30-15)19(26)21-11-10-16-6-8-17(9-7-16)31(28,29)24-20(27)22-25-12-4-2-3-5-13-25/h6-9,14H,2-5,10-13H2,1H3,(H,21,26)(H2,22,24,27) ...
... (CBZ), sold under the trade name Tegretol among others, is an anticonvulsant medication used primarily in the treatment of epilepsy and neuropathic pain.[1] It is not effective for absence or myoclonic seizures.[1] It is used in schizophrenia along with other medications and as a second-line agent in bipolar disorder.[3][1] Carbamazepine appears to work as well as phenytoin and valproate for focal and generalised seizures.[4] Common side effects include nausea and drowsiness.[1] Serious side effects may include skin rashes, decreased bone marrow function, suicidal thoughts, or confusion.[1] It should not be used in those with a history of bone marrow problems.[1] Use during pregnancy may cause harm to the baby; however, stopping the medication in pregnant women with seizures is not recommended.[1] Its use during breastfeeding is not recommended.[1] Care should be taken in those with either kidney or liver problems.[1] Carbamazepine was discovered in 1953 by Swiss chemist Walter ...
A channel that is "inwardly-rectifying" is one that passes current (positive charge) more easily in the inward direction (into the cell) than in the outward direction (out of the cell). It is thought that this current may play an important role in regulating neuronal activity, by helping to stabilize the resting membrane potential of the cell. By convention, inward current (positive charge moving into the cell) is displayed in voltage clamp as a downward deflection, while an outward current (positive charge moving out of the cell) is shown as an upward deflection. At membrane potentials negative to potassium's reversal potential, inwardly rectifying K+ channels support the flow of positively charged K+ ions into the cell, pushing the membrane potential back to the resting potential. This can be seen in figure 1: when the membrane potential is clamped negative to the channel's resting potential (e.g. -60 mV), inward current flows (i.e. positive charge flows into the cell). However, when the ...
... also binds to and blocks α2δ subunit-containing VDCCs, similarly to gabapentin and pregabalin, and hence is a gabapentinoid.[9][16] Both (R)-phenibut and (S)-phenibut display this action with similar affinity (Ki = 23 and 39 μM, respectively).[9] Moreover, (R)-phenibut possesses 4-fold greater affinity for this site than for the GABAB receptor (Ki = 92 μM), while (S)-phenibut does not bind significantly to the GABAB receptor (Ki , 1 mM).[9] As such, based on the results of this study, phenibut would appear to have much greater potency in its interactions with α2δ subunit-containing VDCCs than with the GABAB receptor (between 5- to 10-fold).[9] For this reason, the actions of phenibut as a α2δ subunit-containing voltage-gated calcium channel blocker or gabapentinoid may be its true primary mechanism of action, and this may explain the differences between phenibut and its close relative baclofen (which, in contrast, has essentially insignificant activity as a gabapentinoid; Ki = 6 ...
InChI=1S/C24H34N2O/c1-21(2)19-27-20-24(25-15-9-10-16-25)18-26(23-13-7-4-8-14-23)17-22-11-5-3-6-12-22/h3-8,11-14,21,24H,9-10,15-20H2,1-2H3 ...
... (marketed as Depamide by Sanofi-Aventis) is a carboxamide derivative of valproic acid used in the treatment of epilepsy and some affective disorders. It is rapidly metabolised (80%) to valproic acid (another anticonvulsant) but has anticonvulsant properties itself. It may produce more stable plasma levels than valproic acid or sodium valproate and may be more effective at preventing febrile seizures. However, it is over one hundred times more potent as an inhibitor of liver microsomal epoxide hydrolase. This makes it incompatible with carbamazepine and can affect the ability of the body to remove other toxins. Valpromide is no safer during pregnancy than valproic acid. Valpromide is formed through the reaction of valproic acid and ammonia via an intermediate acid chloride. In pure form, valpromide is a white crystalline powder and has melting point 125-126 °C. It is practically insoluble in water but soluble in hot water. It is available on the market in some European countries. ...
Class Ib antiarrhythmic agents are sodium channel blockers. They have fast onset and offset kinetics, meaning that they have little or no effect at slower heart rates, and more effects at faster heart rates. Class Ib agents shorten the action potential duration and reduce refractoriness. These agents will decrease Vmax in partially depolarized cells with fast response action potentials. They either do not change the action potential duration, or they may decrease the action potential duration. Class Ib drugs tend to be more specific for voltage gated Na channels than Ia. Lidocaine in particular is highly frequency dependent, in that it has more activity with increasing heart rates. This is because lidocaine selectively blocks Na channels in their open and inactive states and has little binding capability in the resting state. Class Ib agents are indicated for the treatment of ventricular tachycardia and symptomatic premature ventricular beats, and prevention of ventricular fibrillation. Class Ib ...
... has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na+ and Ca2+ channels.[1] How this effect is mediated and to what extent this mechanism is involved in the anxiolytic and analgesic effects of kavalactones on the central nervous system is unknown. Kavain's pharmacological activities have not been sufficiently investigated, and neither its effect as a serotonin reuptake inhibitor nor its monoamine (norepinephrine) uptake inhibitions and activation of NMDA receptors have been confirmed. The mechanism behind the psychotropic, sedative, and anxiolytic actions of kavain and related kavalactones is still debated. Direct binding to the benzodiazepine/flumazenil binding site of the GABA-A receptor does not occur with kavain enantiomers.[2] Many studies involved kava extracts from different plant parts and are, therefore, not applicable to kavain itself. In 2016, kavain was shown to bind at the α4β2δ GABAA receptor and ...
... has a potential for drug interactions; caution should be used in combining other medicines with it, including other antiepileptics and mood stabilizers.[12] Lower levels of carbamazepine are seen when administrated with phenobarbital, phenytoin, or primidone, which can result in breakthrough seizure activity. Carbamazepine, as a CYP450 inducer, may increase clearance of many drugs, decreasing their concentration in the blood to subtherapeutic levels and reducing their desired effects.[19] Drugs that are more rapidly metabolized with carbamazepine include warfarin, lamotrigine, phenytoin, theophylline, and valproic acid.[12] Drugs that decrease the metabolism of carbamazepine or otherwise increase its levels include erythromycin,[20] cimetidine, propoxyphene, and calcium channel blockers.[12] Carbamazepine also increases the metabolism of the hormones in birth control pills and can reduce their effectiveness, potentially leading to unexpected pregnancies.[12] As a drug that induces ...
... occludes the pore of calcium-activated voltage-gated shaker K+ channels by binding to one of four independent, overlapping binding sites.[6][7] It binds both to the open and the closed states. In addition, the block is enhanced as the ionic strength is lowered.[8] This block occurs as the Asn 30 on the CTX interacts with the Asp 381 on the K+ channel.[9] The blockade of K+ channels by the charybdotoxin peptide causes neuronal hyperexcitability. Mutations of the Lys31Gln and the Asn30Gln had the effect of lessening the CTX block of the pore on the shaker channel.[9] ...
... has several uses including the treatment of abnormal heart rhythms or arrhythmias, chronic pain, and myotonia. In general when treating arrhythmias, mexiletine is reserved for use in dangerous heart rhythm disturbances such as ventricular tachycardia.[2] It is of particular use when treating arrhythmias caused by long QT syndrome.[3] The LQT3 form of long QT syndrome is amenable to treatment with mexiletine as this form is caused by defective sodium channels that continue to release a sustained current rather than fully inactivating, however other forms of long QT syndrome can also be treated with this medication.[3] Mexiletine has been used to treat chronic pain and may also be used to treat muscle stiffness resulting from myotonic dystrophy (Steinert's disease) or nondystrophic myotonias such as myotonia congenita (Thomsen syndrome or Becker syndrome).[4][5] ...
... is available as a generic medication and usually not too expensive.[7] Wholesale it costs between US$0.003 and US$0.15 per dose.[8] A month of treatment is about US$30 in the United States.[2] Since September 2012, the marketing licence in the UK has been held by Flynn Pharma Ltd, of Dublin, Ireland, and the product, although identical, has been called Phenytoin Sodium xxmg Flynn Hard Capsules. (The xxmg in the name refers to the strength-for example "Phenytoin sodium 25 mg Flynn Hard Capsules").[49] The capsules are still made by Pfizer's Goedecke subsidiary's plant in Freiburg, Germany and they still have Epanutin printed on them.[50] After Pfizer's sale of the UK marketing licence to Flynn Pharma, the price of a 28-pack of 25 mg phenytoin sodium capsules marked Epanutin rose from 66p (about $0.88) to £15.74 (about $25.06). Capsules of other strengths also went up in price by the same factor-2384%,[51] costing the UK's National Health Service an extra £43 million (about $68.44 ...
... is effective for prevention of shivering during surgery or recovery from surgery.[5][6] Nefopam was significantly more effective than aspirin as an analgesic in one clinical trial,[7] although with a greater incidence of side effects such as sweating, dizziness and nausea, especially at higher doses.[8][9] The estimated relative potency of nefopam to morphine indicates that 20 mg of nefopam HCl is the approximate analgesic equal of 12 mg of morphine with comparable analgesic efficacy to morphine,[10][11][12] or oxycodone,[13] while Nefopam tends to produce fewer side effects, does not produce respiratory depression,[14] and has much less abuse potential, and so is useful either as an alternative to opioids, or as an adjunctive treatment for use alongside opioid(s) or other analgesics.[12][15] Nefopam is also used to treat severe hiccups.[16] ...
... is an intermediate chemical in the biosynthesis of ajmaline. Vomilenine reductase--a novel enzyme catalyzing a ... crucial step in the biosynthesis of the therapeutically applied antiarrhythmic alkaloid ajmaline. ...
Hinse C, Stöckigt J (July 2000). "The structure of the ring-opened N beta-propyl-ajmaline (Neo-Gilurytmal) at physiological pH ... Prajmaline is a semi-synthetic propyl derivative of ajmaline, with a higher bioavailability than its predecessor. It acts to ... Sowton E, Sullivan ID, Crick JC (1984). "Acute haemodynamic effects of ajmaline and prajmaline in patients with coronary heart ... is obviously responsible for its better absorption and bioavailability when compared with ajmaline (Gilurytmal)". Die Pharmazie ...
"Properties of vinorine synthase the Rauwolfia enzyme involved in the formation of the ajmaline skeleton". Z. Naturforsch. C: ...
Ajmaline, a class Ia antiarrhythmic agent and Ajmalan a parent hydride, are named after him. After the partition of India ...
... a key enzyme in the biosynthesis of sarpagine/ajmaline type alkaloids". Planta Med. 48 (8): 221-7. doi:10.1055/s-2007-969924. ...
Ruppert M, Woll J, Giritch A, Genady E, Ma X, Stockigt J (2005). "Functional expression of an ajmaline pathway-specific ...
"A newly-detected reductase from Rauvolfia closes a gap in the biosynthesis of the antiarrhythmic alkaloid ajmaline". Planta ...
Medications such as ajmaline may be used to reveal the ECG changes.[2] Similar ECG patterns may be seen in certain electrolyte ... with some suggestions indicating that ajmaline may be the most effective.[23] Precaution must be taken in giving these ... The most commonly used drugs for this purpose are ajmaline, flecainide, and procainamide, ... "Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome". Heart Rhythm. 2 (3): 254-60. doi ...
... the more important being two chemical classes known as the ajmaline and the serpentine group. The quantity of the total ...
A list of US medications equivalent to Ajmaline is available on the Drugs.com website. ... Ajmaline is a medicine available in a number of countries worldwide. ...
... ; Ritmos; 5H-6,10:11,12a-Dimethanoindolo[3,2-b]quinolizine, ajmalan-17,21-diol deriv.; NSC 15627 ...
In both cases, Ajmaline causes the action potential to become longer and ultimately leads to bradycardia. When ajmaline ... Ajmaline also prolongs the QR interval since it can also act as sodium channel blocker, therefore making it take longer for the ... Ajmaline can be found in most species of the Rauvolfia genus as well as Catharanthus roseus. In addition to Southeast Asia, ... Ajmaline was first discovered to lengthen the refractory period of the heart by blocking sodium ion channels, but it has also ...
Tags: buy Ajmaline , Ajmaline supplier , purchase Ajmaline , Ajmaline cost , Ajmaline manufacturer , order Ajmaline , Ajmaline ... Ajmaline, found in the root of Rauwolfia serpentina, is a class Ia antiarrhythmic agent.. ... Ajmaline, found in the root of Rauwolfia serpentina, is a class Ia antiarrhythmic agent. ...
... Author(s): Sorgente, A.; Yazaki, Y.; Capulzini, L.; ... We present an unusual transient pro-arrhythmic effect of ajmaline in a patient with resuscitated cardiac arrest and a left ... possible physio-pathological explanation for this new pro-arrhythmic effect linked to administration of intravenous ajmaline. ...
The preparation of Ajmaline should be 1mg/kg into a 20 ml syringe. Maximum dose is 100 mg. The administration of the drug ... The purpose of the Ajmaline Challenge is to diagnose Brugada Syndrome. ... The purpose of the Ajmaline Challenge is to diagnose Brugada Syndrome.. The preparation of Ajmaline should be 1mg/kg into a 20 ...
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What is a ajmaline challenge?. Ajmaline is a drug known as a sodium channel blocker. It is routinely used by doctors to prevent ... Is the ajmaline challenge safe?. Yes, the ajmaline challenge is safe. However, as with any procedure, there are potential risks ... Why do I need a ajmaline challenge?. Your doctor has advised you to undergo a ajmaline challenge to exclude Brugada syndrome. ... Ajmaline is used by doctors in this test as it blocks the faulty sodium channels and unmasks ECG changes in those patients who ...
The aim of the present study was to evaluate the prevalence of positive ajmaline challenge for BrS in a … ... Ajmaline Testing and the Brugada Syndrome Alessandro Rizzo 1 , Gianluca Borio 1 , Juan Sieira 1 , Sonia Van Dooren 2 , Ingrid ... In non-familial screening group (1,714) ajmaline testing resulted positive in 186 (10.9%). Indications for ajmaline testing ... Ajmaline Testing and the Brugada Syndrome Alessandro Rizzo et al. Am J Cardiol. 2020. . ...
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Lamotrigine is a member of the sodium channel blocking class of antiepileptic drugs.[60] This may suppress the release of glutamate and aspartate, two of the dominant excitatory neurotransmitters in the CNS.[61] It is generally accepted to be a member of the sodium channel blocking class of antiepileptic drugs,[62] but it could have additional actions since it has a broader spectrum of action than other sodium channel antiepileptic drugs such as phenytoin and is effective in the treatment of the depressed phase of bipolar disorder, whereas other sodium channel blocking antiepileptic drugs are not, possibly on account of its sigma receptor activity. In addition, lamotrigine shares few side-effects with other, unrelated anticonvulsants known to inhibit sodium channels, which further emphasises its unique properties.[63] It is a triazine derivate that inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membranes. It also blocks L-, N-, and P-type calcium channels and ...
The hormone prolactin stimulates lactation (production of breast milk). Dopamine, released by the hypothalamus stops the release of prolactin from the pituitary gland. Domperidone, by acting as an anti-dopaminergic agent, results in increased prolactin secretion, and thus promotes lactation (that is, it is a galactogogue). In some nations, including Australia, domperidone is used off-label, based on uncertain and anecdotal evidence of its usefulness, as a therapy for mothers who are having difficulty breastfeeding.[24][25] In the United States, domperidone is not approved for this or any other use.[26][27] A study called the EMPOWER trial was designed to assess the effectiveness and safety of domperidone in assisting mothers of preterm babies to supply breast milk for their infants.[28] The study randomized 90 mothers of preterm babies to receive either domperidone 10 mg orally three times daily for 28 days (Group A) or placebo 10 mg orally three times daily for 14 days followed by domperidone ...
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Ajmaline challenge. Ajmaline (1 mg/kg) was administered intravenously over a 5-min period to unmask the diagnostic ECG pattern ... Ajmaline challenge. From 1992 to 2013, a total of 169 individuals ≤12 years of age underwent an ajmaline challenge for ... Among them, ajmaline challenge revealed a Brugada ECG type 1 in 40 children (24%). ECG parameters before and after ajmaline ... Ajmaline challenge. Ajmaline challenge is an established tool to unmask the diagnostic Brugada ECG pattern in patients with ...
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Check with your doctor if you used this medicine and your migraine did not go away, or if your migraine got worse or started occurring more often. This medicine may increase your risk of having abnormal heart rhythm, heart attack, angina, or stroke. This is more likely to occur if you or a family member already has heart disease, if you have diabetes, high blood pressure, or if you smoke. Call your doctor right away if you have any symptoms of a heart problem, such as chest pain or discomfort, an uneven heartbeat, nausea or vomiting, pain or discomfort in the shoulders, arms, jaw, back, or neck, shortness of breath, or sweating. Call your doctor right away if you have any symptoms of a stroke, such as confusion, difficulty with speaking, double vision, headaches, an inability to move the arms, legs, or facial muscles, an inability to speak, or slow speech. Check with your doctor right away if you have chest discomfort, jaw or neck tightness after taking this medicine. Also, tell your doctor if ...
This medicine will add to the effects of alcohol and other CNS depressants (medicines that make you drowsy or less alert). Some examples of CNS depressants are antihistamines or medicine for allergies or colds, sedatives, tranquilizers, or sleeping medicine, prescription pain medicine or narcotics, medicine for seizures or barbiturates, muscle relaxants, or anesthetics, including some dental anesthetics. Check with your doctor before taking any of the above while you are using this medicine. This medicine may cause some people to become dizzy, drowsy, or may cause trouble with thinking or controlling body movements, which may lead to falls, fractures or other injuries. Even if you take haloperidol at bedtime, you may feel drowsy or less alert on arising. Make sure you know how you react to this medicine before you drive, use machines, or do anything else that could be dangerous if you are dizzy or not alert. Dizziness, lightheadedness, or fainting may occur, especially when you get up from a ...
Ajmaline 17-(Chloroacetate) Monohydrochloride. Drug: Ajmaline 17-(Chloroacetate) Monohydrochloride Ajmaline 17-(Chloroacetate) ... Ajmaline 17-(Chloroacetate) Monohydrochloride. Drug: Ajmaline 17-(Chloroacetate) Monohydrochloride Ajmaline 17-(Chloroacetate) ... Ajmaline. Lorajmine. Anti-Arrhythmia Agents. Voltage-Gated Sodium Channel Blockers. Sodium Channel Blockers. Membrane Transport ... All consecutive patients with suspected BrS-ECG pattern will perform an ajmaline testing (1mg/kg in 5 min). A total of 30 ...
The monomeric units belong to the sarpagine, ajmaline, macroline, vobasine, and pleiocarpamine series. An up-to-date discussion ... The monomeric units belong to the sarpagine, ajmaline, macroline, vobasine, and pleiocarpamine series. An up-to-date discussion ... Keywords: Alstonia genus; Apocynaceae family; sarpagine; macroline; ajmaline; bisindole alkaloids; biomimetic synthesis; ... ajmaline; bisindole alkaloids; biomimetic synthesis; partial and total synthesis; enantiospecific and regiospecific synthesis ...
Immunological protection against ajmaline toxicity.. Descotes J, Cadot R, Evreux JC, Grenot C, Cuilleron CY. ...
Ajmaline test Q&A with Dr Michael Papadakis. Dr Michael Papadakis answers some of your questions about their recent research ... Characterization of early repolarization during ajmaline provocation and exercise tolerance testing. Bastiaenen, R., Raju, H., ... "Characterization of early repolarization during ajmaline provocation and exercise tolerance testing." Heart Rhythm October 2012 ... death to the CRY Centre for Inherited Cardiac Conditions at St Georges Hospital would they always/usually have the ajmaline ...
Omega, delta and kappa families of conotoxins have a knottin or inhibitor cystine knot scaffold. The knottin scaffold is a very special disulfide-through-disulfide knot, in which the III-VI disulfide bond crosses the macrocycle formed by two other disulfide bonds (I-IV and II-V) and the interconnecting backbone segments, where I-VI indicates the six cysteine residues starting from the N-terminus. The cysteine arrangements are the same for omega, delta and kappa families, even though omega conotoxins are calcium channel blockers, whereas delta conotoxins delay the inactivation of sodium channels, and kappa conotoxins are potassium channel blockers.[7] ...
Importantly, our data emphasize the potential for confounding possibly false-positive ajmaline responses in this population, ... a positive ajmaline response was observed in a large proportion of UCA/SUD families. ... Ventricular arrhythmia during ajmaline challenge for the Brugada syndrome. Dobbels B, De Cleen D, Ector J. Dobbels B, et al. ... We assessed ajmaline test response and genetic testing results in 637 individuals from 482 families who underwent ajmaline ...
FlecainideBrugada SyndromeReserpineAlkaloidsAssessed ajmaline testUnderwentHakim AjmaPROVOCATION TESTUnmaskRauvolfiaElectrocardiogramSerpentinaAlkaloidArrhythmiaSodium channel blockerCardiac arrestPrajmalineChallengeDiagnosisSymptomsPatients with suspectedCharacteristicAdministrationClinicalTestingPositiveSlowlySearchIndividualsRiskNegativeTypeAction
- Effects of as sodium blocking drugs such as Ajmaline, Ethacizin, and Flecainide. (medindia.net)
- Ajmaline test" is used throughout to describe the use of intravenous sodium channel blockers to unravel a type 1 Brugada ECG and diagnose Brugada syndrome, with the understanding that flecainide, pilsicainide, and procainamide are used in different countries for the same purpose. (onlinejacc.org)
- Beta-adrenergic stimulation normalizes the ECG, while IV ajmaline, flecainide or procainamide accentuate the ST segment elevation and are capable of unmasking concealed and intermittent forms of the disease. (fac.org.ar)
- Some family members only manifest the typical ECG pattern after ajmaline or flecainide administration. (fac.org.ar)
- Recent studies 2-4 have reported that class I antiarrhythmic drugs such as flecainide, procainamide, and ajmaline could unmask ST segment elevation in patients with "latent" Brugada syndrome. (bmj.com)
- Agents that dissociate slowly from the sodium channel such as flecainide and ajmaline unmask the Brugada syndrome electrocardiogram and precipitate ventricular tachycardia/fibrillation. (ahajournals.org)
- 3,4 Sodium channel blockers with slow dissociation kinetics such as flecainide and ajmaline are known to unmask the BrS ECG phenotype as well as precipitating ventricular tachycardia/fibrillation. (ahajournals.org)
- Ajmaline is used intravenously to test for Brugada syndrome since they both affect the sodium ion channel. (wikipedia.org)
- The purpose of the Ajmaline Challenge is to diagnose Brugada Syndrome. (brave-study.org)
- Your doctor suspects that you may have Brugada syndrome and he has advised you to have a simple test known as a ajmaline challenge to confirm the diagnosis. (heartrhythmclinic.com)
- Your doctor has advised you to undergo a ajmaline challenge to exclude Brugada syndrome. (heartrhythmclinic.com)
- The study purpose is to evaluate the morphological and functional characteristics of the right ventricle before and after ajmaline in patients diagnosed with Brugada syndrome. (clinicaltrials.gov)
- Ajmaline testing to diagnose Brugada syndrome (BrS) is routinely used in the evaluation of SUD and UCA, but its yield, limitations, and appropriate dosing have not been studied in a large cohort. (cdc.gov)
- Testing using ajmaline (an alkaloid) challenge is recommended, as it is an antiarrhythmic agent that can bring out the diagnostic electrocardiogram (ECG) pattern typical in patients suspected of having Brugada syndrome. (eurekalert.org)
- The study included 53 asymptomatic individuals with a first-degree relative with Brugada syndrome and negative ajmaline test performed before 16 years of age between 1992 and 2010 who were seen at the university hospital of Brussels, Belgium (UZ Brussel- VUB) and had an ECG repeated annually and were scheduled to repeat the test after puberty. (eurekalert.org)
- We sought to identify predictors of ajmaline-induced PR and QRS changes and Type I Brugada syndrome (BrS) electrocardiogram (ECG). (eur.nl)
- We calculated polygenic risk scores (PRS) for PR interval (PRSPR), QRS duration (PRSQRS), and Brugada syndrome (PRSBrS) derived from published genome-wide association studies and used regression analysis to identify predictors of ajmaline dose related PR change (slope) and QRS slope. (eur.nl)
- At the same time, 1 in 5 patients undergoing ICD implantation for Brugada syndrome in Europe are asymptomatic and had "their Brugada syndrome" diagnosed by virtue of a positive ajmaline test (1) . (onlinejacc.org)
- Clearly, we continue to diagnose asymptomatic young male subjects as "Brugada syndrome" (essentially implying a diagnosis of congenital Brugada syndrome), when they develop a type 1 Brugada electrocardiogram (ECG) in response to an ajmaline test (2) . (onlinejacc.org)
- In fact, among patients diagnosed with Brugada syndrome in the absence of symptoms, the percentage of patients with an ajmaline-based diagnosis increased significantly over the last decade from 50% to 74% (3) . (onlinejacc.org)
- Undeniably, the fact that the ajmaline test is perceived as ≈100% specific for diagnosing Brugada syndrome (5) led to the collective belief that all patients with a positive ajmaline test have Brugada syndrome. (onlinejacc.org)
- By the present guidelines, a positive ajmaline confers an unequivocal diagnosis of Brugada syndrome (2) , whereas a more recent consensus report grants a diagnosis of probable Brugada syndrome to asymptomatic patients when a positive ajmaline test is the only positive criteria (6) . (onlinejacc.org)
- Importantly, a confounding ajmaline test, representing a positive ajmaline test in individuals who, to the best judgment of the investigators, do not have Brugada syndrome, were found in 8% of families undergoing this test (8) . (onlinejacc.org)
- While 86 alkaloids have been discovered throughout Rauvolfia vomitoria, ajmaline is mainly isolated from the stem bark and roots of the plant. (wikipedia.org)
- Over seventy macroline/sarpagine/ajmaline related alkaloids have been isolated from species of Alstonia. (uwm.edu)
- We assessed ajmaline test response and genetic testing results in 637 individuals from 482 families who underwent ajmaline testing for SUD or UCA. (cdc.gov)
- The aim of the present study was to evaluate the prevalence of positive ajmaline challenge for BrS in a cohort of consecutive patients who underwent electrophysiological evaluation for different clinical reasons. (cdc.gov)
- All consecutive patients from 2008 to 2019 who underwent ajmaline testing were prospectively included. (cdc.gov)
- A total of 2,456 patients underwent ajmaline testing, 742 (30.2%) in the context of familial screening for BrS. (cdc.gov)
- METHODS AND RESULTS: In 1368 patients that underwent ajmaline infusion for suspected BrS, we performed measurements of 26 721 ECGs, dose-response mixed modelling and genotyping. (eur.nl)
- The 12-lead ECGs of 117 individual members, who underwent comprehensive cardiac investigations including an Ajmaline provocation test, when appropriate, were reviewed. (ahajournals.org)
- He named it ajmaline, after Hakim Ajmal Khan, one of the most illustrious practitioners of Unani medicine in South Asia. (wikipedia.org)
- He named the newly discovered chemical compound as Ajmaline, after his mentor Hakim Ajmal Khan who was one of the illustrious practitioners of Unani system of medicine in South Asia. (wikipedia.org)
- Only 6 (16%) subjects exhibited a diagnostic baseline ECG, while the great majority required an Ajmaline provocation test to unmask the Brugada phenotype. (ahajournals.org)
- Pharmacological challenge with ajmaline, a potent sodium channel blocker with a short half-life, is the recommended test to unmask the diagnostic Brugada electrocardiogram (ECG) pattern in patients with suspected BS and nondiagnostic ECG (2) . (onlinejacc.org)
- Ajmaline can be found in most species of the Rauvolfia genus as well as Catharanthus roseus. (wikipedia.org)
- Ajmaline is an antiarrhythmic agent produced by the plant Rauvolfia serpentina . (metacyc.org)
- In an afflicted person who was induced with ajmaline, the electrocardiogram would show the characteristic pattern of the syndrome where the ST segment is abnormally elevated above the baseline. (wikipedia.org)
- Ajmaline, found in the root of Rauwolfia serpentina, is a class Ia antiarrhythmic agent. (selleckchem.com)
- Enzymatic biosynthesis of vomilenine, a key intermediate of the ajmaline pathway, catalysed by a novel cytochrome P-450-dependent enzyme from plant cell cultures of Rauwolfia serpentina. (genome.jp)
- Ajmaline (also known by trade names Gilurytmal, Ritmos, and Aritmina) is an alkaloid that is class Ia antiarrhythmic agent. (wikipedia.org)
- Forms a stage in the biosynthesis of the indole alkaloid ajmaline. (genome.jp)
- The ECG will record how your heart reacts to ajmaline, this allows your doctor to collect detailed information about the cause of your potential arrhythmia. (heartrhythmclinic.com)
- Very rarely, in less than 1% of patients the ajmaline may cause your heart to go into a very fast ventricular rhythm, if this happens the doctor will need to correct your arrhythmia quickly by cardioversion. (heartrhythmclinic.com)
- There is a very low risk that you may experience an arrhythmia after the ajmaline has finished. (heartrhythmclinic.com)
- Ajmaline also prolongs the QR interval since it can also act as sodium channel blocker, therefore making it take longer for the membrane to depolarize in the first case. (wikipedia.org)
- Ajmaline is a drug known as a sodium channel blocker. (heartrhythmclinic.com)
- We present an unusual transient pro-arrhythmic effect of ajmaline in a patient with resuscitated cardiac arrest and a left ventricular apical aneurysm. (ru.nl)
- This study evaluated the yield of ajmaline testing and assessed the occurrence of confounding responses in a large cohort of families with unexplained cardiac arrest (UCA) or sudden unexplained death (SUD). (cdc.gov)
- (8) reviewed the results of 637 ajmaline tests performed on 54 probands with unexplained cardiac arrest and on 583 family members. (onlinejacc.org)
- In total, 14% of all ajmaline tests performed were positive, including 20% of the tests of cardiac arrest survivors. (onlinejacc.org)
- Due to the low bioavailability of ajmaline, a semisynthetic propyl derivative called prajmaline (trade name Neo-gilurythmal) was developed that induces similar effects to its predecessor but has better bioavailability and absorption. (wikipedia.org)
- Due to complications that could arise with the ajmaline challenge, a specialized nurse should perform the administration and have an emergency defibrillator nearby. (wikipedia.org)
- Why do I need a ajmaline challenge? (heartrhythmclinic.com)
- Ajmaline challenge is a well-established clinical test. (heartrhythmclinic.com)
- What is a ajmaline challenge? (heartrhythmclinic.com)
- The ajmaline challenge is undertaken in a ward setting with cardiac monitoring. (heartrhythmclinic.com)
- Is the ajmaline challenge safe? (heartrhythmclinic.com)
- The ajmaline challenge is performed safely in both children and adults. (heartrhythmclinic.com)
- Relatives developing symptoms should always be investigated with ajmaline challenge even if they had a negative drug test performed before puberty. (eurekalert.org)
- Methods Among 505 patients with ajmaline-induced BS, subjects ≤12 years of age at the time of diagnosis were considered as children and eligible for this study. (onlinejacc.org)
- Ajmaline test confirmed the BrS diagnosis. (frontiersin.org)
- Ajmaline was seen to be more effective than lidocaine (an accepted drug for treatment) in terminating ventricular tachycardia for acute treatment or emergency therapy for people with recurring symptoms. (wikipedia.org)
- All consecutive patients with suspected BrS-ECG pattern will perform an ajmaline testing (1mg/kg in 5 min). (clinicaltrials.gov)
- The purpose of the test is to use a drug called ajmaline to uncover the characteristic ECG changes. (heartrhythmclinic.com)
- We discuss the clinical presentation and the possible physio-pathological explanation for this new pro-arrhythmic effect linked to administration of intravenous ajmaline. (ru.nl)
- It is common to experience a metallic taste in your mouth during the administration of the ajmaline. (heartrhythmclinic.com)
- The effects of ajmaline in experimental and clinical arrhythmias and their relation to some electrophysiological parameters of the heart. (aspetjournals.org)
- A total of 60 selected subjects (30 patients with positive ajmaline testing and 30 with negative testing) will be enrolled. (clinicaltrials.gov)
- Dr Michael Papadakis answers some of your questions about their recent research publication identifying the importance of routine ajmaline testing after a SADS death. (c-r-y.org.uk)
- Considering the renowned expertise of the investigators, it is fair to say that these "confounding ajmaline tests" simply represent false-positive test results. (onlinejacc.org)
- When ajmaline reversibly blocks hERG, repolarization occurs more slowly because it is harder for potassium to get out due to less unblocked channels, therefore making the RS interval longer. (wikipedia.org)
- Listing your company for AJMALINE - PHYTOCHEMICALS allows buyers to find your information through our directory pages which appear in the top positions when a search is conducted in Google, Yahoo! (poulvet.com)
- The remaining 43 individuals repeated the ajmaline test, which unmasked type 1 ECG in 10 patients (23 percent). (eurekalert.org)
- Children are at higher risk of ajmaline-induced VAs. (onlinejacc.org)
- In both cases, Ajmaline causes the action potential to become longer and ultimately leads to bradycardia. (wikipedia.org)
- Ajmaline causes action potentials to be prolonged, therefore slowing down firing of the conducting myocytes which ultimately slows the beating of the heart. (wikipedia.org)