A C19 norditerpenoid alkaloid (DITERPENES) from the root of ACONITUM plants. It activates VOLTAGE-GATED SODIUM CHANNELS. It has been used to induce ARRHYTHMIAS in experimental animals and it has antiinflammatory and antineuralgic properties.
A plant genus of the family RANUNCULACEAE. Members contain a number of diterpenoid alkaloids including: aconitans, hypaconitine, ACONITINE, jesaconitine, ignavine, napelline, and mesaconitine. The common name of Wolfbane is similar to the common name for ARNICA.
A benzoate-cevane found in VERATRUM and Schoenocaulon. It activates SODIUM CHANNELS to stay open longer than normal.
A class of drugs that stimulate sodium influx through cell membrane channels.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
Batrachotoxin is the 20-alpha-bromobenzoate of batrachotoxin A; they are toxins from the venom of a small Colombian frog, Phyllobates aurotaenia, cause release of acetylcholine, destruction of synaptic vesicles and depolarization of nerve and muscle fibers.
Organic nitrogenous bases. Many alkaloids of medical importance occur in the animal and vegetable kingdoms, and some have been synthesized. (Grant & Hackh's Chemical Dictionary, 5th ed)
The study of the origin, nature, properties, and actions of drugs and their effects on living organisms.
A nucleus of the middle hypothalamus, the largest cell group of the tuberal region with small-to-medium size cells.
An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.
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.
Chinese herbal or plant extracts which are used as drugs to treat diseases or promote general well-being. The concept does not include synthesized compounds manufactured in China.

Synaptic transmission at nicotinic acetylcholine receptors in rat hippocampal organotypic cultures and slices. (1/219)

1. Whole-cell clamp recordings of the compound synaptic current elicited by afferent stimulation of Schaffer collaterals showed that blockade of the NMDA, AMPA and GABAA receptor-mediated components by 6-nitro-7-sulphamoyl- benzo(f)quinoxaline-2,3-dione (NBQX), 3-((R)-2-carboxypiperazine-4-yl)propyl-1-phosphonate (R-CPP) and picrotoxin, respectively, left a small residual current in 39 out of 41 CA1 pyramidal neurones in organotypic cultures and 9 out of 16 CA1 cells in acutely prepared slices. 2. This current represented 2. 9 +/- 0.4 % of the compound evoked synaptic response in organoypic cultures and 1.4 +/- 0.5 % in slices. It was characterized by a slightly rectifying I-V curve and a reversal potential of 3.4 +/- 5. 1 mV. 3. This residual current was insensitive to blockers of GABAB, purinergic, muscarinic and 5-HT3 receptors, but it was essentially blocked by the nicotinic receptor antagonist d-tubocurarine (91 +/- 4 % blockade; 20 microM), and partly blocked by alpha-bungarotoxin (200 nM) and methyllycaconitine (10 nM), two antagonists with a higher selectivity for alpha7 subunit-containing nicotinic receptors (48 +/- 3 % and 55 +/- 11 % blockade, respectively). 4. The residual current was of synaptic origin, since it occurred after a small delay; its amplitude depended upon the stimulation intensity and it was calcium dependent and blocked by the sodium channel antagonist tetrodotoxin. 5. We conclude that afferent stimulation applied in the stratum radiatum evokes in some hippocampal neurones a small synaptic current mediated by activation of neuronal nicotinic receptors.  (+info)

Nicotinic acetylcholine receptors assembled from the alpha7 and beta3 subunits. (2/219)

Intracellular recordings were performed in voltage-clamped Xenopus oocytes upon injection with a mixture of cDNAs encoding the beta3 and mutant alpha7 (L247Talpha7) neuronal nicotinic acetylcholine receptor (nAChR) subunits. The expressed receptors maintained sensitivity to methyllycaconitine and to alpha-bungarotoxin but exhibited a functional profile strikingly different from that of the homomeric L247Talpha7 receptor. The heteromeric L247Talpha7beta3 nAChR had a lower apparent affinity and a faster rate of desensitization than L247Talpha7 nAChR, exhibited nonlinearity in the I-V relationship, and was inhibited by 5-hydroxytryptamine, much like wild type alpha7 (WTalpha7) nAChR. Single channel recordings in cell-attached mode revealed unitary events with a slope conductance of 19 picosiemens and a lifetime of 5 ms, both values being much smaller than those of the homomeric receptor channel. Upon injection with a mixture of WTalpha7 and beta3 cDNAs, clear evidence was obtained for the plasma membrane assembly of heteromeric nAChRs, although ACh could not activate these receptors. It is concluded that beta3, long believed to be an orphan subunit, readily co-assembles with other subunits to form heteromeric receptors, some of which may be negative regulators of cholinergic function.  (+info)

Effects of Delphinium alkaloids on neuromuscular transmission. (3/219)

The Delphinium alkaloids methyllycaconitine (MLA), nudicauline, 14-deacetylnudicauline (14-DN), barbinine, and deltaline were investigated for their effects on neuromuscular transmission in lizards. The substituent at C14 provides the only structural difference among the alkaloids MLA, nudicauline, 14-DN, and barbinine. Deltaline lacks the N-(methylsuccinyl)anthranilic acid at C18 common to the other four alkaloids. Each alkaloid reversibly reduced extracellularly recorded compound muscle action potential (CMAP) amplitudes in a concentration-dependent manner. The IC(50) values for CMAP blockade were between 0.32 and 13.2 microM for the N-(methylsuccinimido)anthranoyllycacotonine-type alkaloids and varied with the C14 moiety; the IC(50) value for deltaline was 156 microM. The slopes of the concentration-response curves for CMAP blockade were similar for each alkaloid except barbinine, whose shallower curve suggested alternative or additional mechanisms of action. Each alkaloid reversibly reduced intracellularly recorded spontaneous, miniature end-plate potential (MEPP) amplitudes. Alkaloid concentrations producing similar reductions in MEPP amplitude were 0.05 microM for 14-DN, 0.10 microM for MLA, 0.50 microM for barbinine, and 20 microM for deltaline. Only barbinine altered the time constant for MEPP decay, further suggesting additional or alternative effects for this alkaloid. MLA and 14-DN blocked muscle contractions induced by exogenously added acetylcholine. All five alkaloids are likely nicotinic receptor antagonists that reduce synaptic efficacy and block neuromuscular transmission. The substituent at C14 determines the potency and possibly the mechanism of nicotinic acetylcholine receptor blockade for MLA, nudicauline, 14-DN, and barbinine at neuromuscular synapses. The lower potency of deltaline indicates that the N-(methylsuccinyl)anthranilic acid at C18 affects alkaloid interactions with nicotinic acetylcholine receptors at neuromuscular junctions.  (+info)

Cooperative activation of action potential Na+ ionophore by neurotoxins. (4/219)

Four neurotoxins that activate the action potential Na+ ionophore of electrically excitable neuroblastoma cells interact with two distinct classes of sites, one specific for the alkaloids veratridine, batrachotoxin, and aconitine, and the second specific for scorpion toxin. Positive heterotropic cooperativity is observed between toxins bound at these two classes of sites. Tetrodotoxin is a noncompetitive inhibitor of activation by each of these toxins (KI = 4-8 nM). These results suggest the existence of three functionally separable components of the action potential Na+ ionophore: two regulatroy components, which bind activating neurotoxins and interact allosterically in controlling the activity of a third ion-transport component, which binds tetrodotoxin.  (+info)

Nicotinic receptor activation in human cerebral cortical interneurons: a mechanism for inhibition and disinhibition of neuronal networks. (5/219)

Cholinergic control of the activity of human cerebral cortical circuits has long been thought to be accounted for by the interaction of acetylcholine (ACh) with muscarinic receptors. Here we report the discovery of functional nicotinic receptors (nAChRs) in interneurons of the human cerebral cortex and discuss the physiological and clinical implications of these findings. The whole-cell mode of the patch-clamp technique was used to record responses triggered by U-tube application of the nonselective agonist ACh and of the alpha7-nAChR-selective agonist choline to interneurons visualized by means of infrared-assisted videomicroscopy in slices of the human cerebral cortex. Choline induced rapidly desensitizing whole-cell currents that, being sensitive to blockade by methyllycaconitine (MLA; 50 nM), were most likely subserved by an alpha7-like nAChR. In contrast, ACh evoked slowly decaying whole-cell currents that, being sensitive to blockade by dihydro-beta-erythroidine (DHbetaE; 10 microM), were most likely subserved by an alpha4beta2-like nAChR. Application of ACh (but not choline) to the slices also triggered GABAergic postsynaptic currents (PSCs). Evidence is provided that ACh-evoked PSCs are the result of activation of alpha4beta2-like nAChRs present in preterminal axon segments and/or in presynaptic terminals of interneurons. Thus, nAChRs can relay inhibitory and/or disinhibitory signals to pyramidal neurons and thereby modulate the activity of neuronal circuits in the human cerebral cortex. These mechanisms, which appear to be retained across species, can account for the involvement of nAChRs in cognitive functions and in certain neuropathological conditions.  (+info)

Anti-arrhythmic effects of sophoridine and oxysophoridine. (6/219)

AIM: To compare the effects of oxysophoridine (Oxy) and sophoridine (Sop) on experimental arrhythmias and myocardial physiologic properties. METHODS: Arrhythmias were induced by drugs and myocardial ischemia. Physiologic properties were determined on isolated heart atria. RESULTS: Oxy 500 mg.kg-1 (1/6 LD50) decreased the incidence of ventricular arrhythmias induced by aconitine (P < 0.01), increased the threshold dose of ouabain-induced ventricular premature (VP, P < 0.05), ventricular tachycardia (VT, P < 0.05), ventricular fibrillation (VF, P < 0.01), and cardiac arrest, (P < 0.01). After i.v. Oxy 500 mg.kg-1 into the rats with ligation of left anterior descending coronary artery, the total numbers of ectopic beats were decreased (P < 0.05), the incidence of VF was lowered, and the duration of VT was shortened (P < 0.01). Oxy 250 mg.kg-1 (1/13 LD50) i.v. shortened the duration of arrhythmias induced by BaCl2 (P < 0.01) and delayed the onset of arrhythmias induced by chloroform-epinephrine (P < 0.05). Oxy produced dose-dependent positive inotropic effects in the isolated left atrial of guinea pigs, increased the concentration of epinephrine to elicit automaticity in left atria, decreased slightly the excitability, and prolonged the functional refractory period. Sop produced the similar effects on arrhythmias as Oxy. CONCLUSION: Oxy produced the similar anti-arrhythmic effects as Sop did at the equivalent effective dose.  (+info)

Inhibition and disinhibition of pyramidal neurons by activation of nicotinic receptors on hippocampal interneurons. (7/219)

Nicotinic acetylcholine receptors (nAChRs) are expressed in the hippocampus, and their functional roles are beginning to be delineated. The effect of nAChR activation on the activity of both interneurons and pyramidal neurons in the CA1 region was studied in rat hippocampal slices. In CA1 stratum radiatum with muscarinic receptors inhibited, local pressure application of acetylcholine (ACh) elicited a nicotinic current in 82% of the neurons. The majority of the ACh-induced currents were sensitive to methyllycaconitine, which is a specific inhibitor of alpha7-containing nAChRs. Methyllycaconitine-insensitive nicotinic currents also were present as detected by a nonspecific nAChR inhibitor. The ACh-sensitive neurons in the s. radiatum were identified as GABAergic interneurons by their electrophysiological properties. Pressure application of ACh induced firing of action potentials in approximately 70% of the interneurons. The ACh-induced excitation of interneurons could induce either inhibition or disinhibition of pyramidal neurons. The inhibition was recorded from the pyramidal neuron as a burst of GABAergic synaptic activity. That synaptic activity was sensitive to bicuculline, indicating that GABA(A) receptors mediated the ACh-induced synaptic currents. The disinhibition was recorded from the pyramidal neuron as a reduction of spontaneous GABAergic synaptic activity when ACh was delivered onto an interneuron. Both the inhibition and disinhibition were sensitive to either methyllycaconitine or mecamylamine, indicating that activation of nicotinic receptors on interneurons was necessary for the effects. These results show that nAChRs are capable of regulating hippocampal circuits by exciting interneurons and, subsequently, inhibiting or disinhibiting pyramidal neurons.  (+info)

Two distinct classes of functional 7-containing nicotinic receptor on rat superior cervical ganglion neurons. (8/219)

Nicotinic acetylcholine receptors (nAChRs) that bind alpha-bungarotoxin (alpha Bgt) were studied on isolated rat superior cervical ganglion (SCG) neurons using whole-cell patch clamp recording techniques. Rapid application of ACh onto the soma of voltage clamped neurons evoked a slowly desensitizing current that was reversibly blocked by alpha Bgt (50 nM). The toxin-sensitive current constituted on average about half of the peak whole-cell response evoked by ACh. Nanomolar concentrations of methyllycaconitine blocked the alpha Bgt-sensitive component of the ACh-evoked current as did intracellular dialysis with an anti-alpha 7 monoclonal antibody. The results indicate that the slowly reversible toxin-sensitive response elicited by ACh arises from activation of an unusual class of alpha 7-containing receptor (alpha 7-nAChR) similar to that reported previously for rat intracardiac ganglion neurons. A second class of functional alpha 7-nAChR was identified on some SCG neurons by using rapid application of choline to elicit responses. In these cases a biphasic response was obtained, which included a rapidly desensitizing component that was blocked by alpha Bgt in a pseudo-irreversible manner. The pharmacology and kinetics of the responses resembled those previously attributed to alpha 7-nAChRs in a number of other neuronal cell types. Experiments measuring the dissociation rate of 125I-labelled alpha Bgt from SCG neurons revealed two classes of toxin-binding site. The times for toxin dissociation were consistent with those required to reverse blockade of the two kinds of alpha Bgt-sensitive response. These results indicate that rat SCG neurons express two types of functional alpha 7-nAChR, differing in pharmacology, desensitization and reversibility of alpha Bgt blockade.  (+info)

Aconitine is a toxic alkaloid compound that can be found in various plants of the Aconitum genus, also known as monkshood or wolf's bane. It is a highly poisonous substance that can cause serious medical symptoms, including numbness, tingling, and paralysis of the muscles, as well as potentially life-threatening cardiac arrhythmias and seizures. Aconitine works by binding to sodium channels in nerve cells, causing them to become overactive and leading to the release of large amounts of neurotransmitters.

In medical contexts, aconitine is not used as a therapeutic agent due to its high toxicity. However, it has been studied for its potential medicinal properties, such as its analgesic and anti-inflammatory effects. Despite these potential benefits, the risks associated with using aconitine as a medicine far outweigh any possible advantages, and it is not considered a viable treatment option.

Aconitum, also known as monkshood or wolf's bane, is a genus of extremely poisonous plants belonging to the family Ranunculaceae. These plants are native to the mountainous regions of the Northern Hemisphere, especially in Asia. The name Aconitum comes from the Greek word "akonitos," which is believed to be derived from "akone," meaning "dart" or "pointed stake," referring to the shape of the plant's roots and its use as a poison on weapons.

The plants contain various alkaloids, primarily aconitine, which is responsible for their toxicity. All parts of the plant are considered poisonous, but the roots and seeds contain the highest concentration of aconitine. Ingesting or touching any part of the Aconitum plant can cause severe symptoms, including nausea, vomiting, diarrhea, heart problems, paralysis, and even death if not treated promptly.

In traditional medicine, some species of Aconitum have been used in small, controlled doses to treat various ailments, such as pain, inflammation, and heart conditions. However, due to the high risk of toxicity, these uses are generally discouraged in modern medicine, and safer alternatives are recommended.

Veratridine is not a medical term, but it is a chemical compound that has been used in scientific research. It's a plant alkaloid found primarily in the seeds and roots of various Veratrum species (also known as false hellebore or white hellebore).

In a pharmacological context, veratridine can be defined as:

A steroidal alkaloid that acts as a potent agonist at voltage-gated sodium channels in excitable membranes. It causes persistent activation of these channels, leading to sustained depolarization and increased neuronal excitability. Veratridine has been used in research to study the properties and functions of sodium channels, as well as neurotransmission and nerve impulse transmission.

However, it is not a term typically used in clinical medicine or patient care.

Sodium channel agonists are substances that enhance the activity or function of sodium channels. Sodium channels are membrane proteins that play a crucial role in the generation and transmission of electrical signals in excitable cells, such as nerve and muscle cells. They allow the influx of sodium ions into the cell, which leads to the depolarization of the cell membrane and the initiation of an action potential.

Sodium channel agonists increase the likelihood, duration, or amplitude of action potentials by promoting the opening of sodium channels or slowing their closure. These effects can have various physiological consequences depending on the type of cell and tissue involved. In some cases, sodium channel agonists may be used for therapeutic purposes, such as in the treatment of certain types of heart arrhythmias. However, they can also have harmful or toxic effects, especially when used in excessive amounts or in sensitive populations.

Examples of sodium channel agonists include some drugs used to treat cardiac arrhythmias, such as Class I antiarrhythmic agents like ajmaline, flecainide, and procainamide. These drugs bind to the sodium channels and stabilize their open state, reducing the frequency and velocity of action potentials in the heart. Other substances that can act as sodium channel agonists include certain neurotoxins, such as batrachotoxin and veratridine, which are found in some species of plants and animals and can have potent effects on nerve and muscle function.

Cardiac arrhythmias are abnormal heart rhythms that result from disturbances in the electrical conduction system of the heart. The heart's normal rhythm is controlled by an electrical signal that originates in the sinoatrial (SA) node, located in the right atrium. This signal travels through the atrioventricular (AV) node and into the ventricles, causing them to contract and pump blood throughout the body.

An arrhythmia occurs when there is a disruption in this electrical pathway or when the heart's natural pacemaker produces an abnormal rhythm. This can cause the heart to beat too fast (tachycardia), too slow (bradycardia), or irregularly.

There are several types of cardiac arrhythmias, including:

1. Atrial fibrillation: A rapid and irregular heartbeat that starts in the atria (the upper chambers of the heart).
2. Atrial flutter: A rapid but regular heartbeat that starts in the atria.
3. Supraventricular tachycardia (SVT): A rapid heartbeat that starts above the ventricles, usually in the atria or AV node.
4. Ventricular tachycardia: A rapid and potentially life-threatening heart rhythm that originates in the ventricles.
5. Ventricular fibrillation: A chaotic and disorganized electrical activity in the ventricles, which can be fatal if not treated immediately.
6. Heart block: A delay or interruption in the conduction of electrical signals from the atria to the ventricles.

Cardiac arrhythmias can cause various symptoms, such as palpitations, dizziness, shortness of breath, chest pain, and fatigue. In some cases, they may not cause any symptoms and go unnoticed. However, if left untreated, certain types of arrhythmias can lead to serious complications, including stroke, heart failure, or even sudden cardiac death.

Treatment for cardiac arrhythmias depends on the type, severity, and underlying causes. Options may include lifestyle changes, medications, cardioversion (electrical shock therapy), catheter ablation, implantable devices such as pacemakers or defibrillators, and surgery. It is essential to consult a healthcare professional for proper evaluation and management of cardiac arrhythmias.

Batrachotoxins are a type of steroidal alkaloid toxin that are found in certain species of frogs, beetles, and plants. They are highly toxic and cause rapid excitation of nerve and muscle tissue leading to paralysis and death. Batrachotoxins work by irreversibly binding to and opening sodium ion channels in cell membranes, causing a persistent depolarization of the membrane potential. This leads to uncontrolled firing of action potentials in nerves and muscles, resulting in the symptoms mentioned above. These toxins are considered among the most potent natural poisons known.

Alkaloids are a type of naturally occurring organic compounds that contain mostly basic nitrogen atoms. They are often found in plants, and are known for their complex ring structures and diverse pharmacological activities. Many alkaloids have been used in medicine for their analgesic, anti-inflammatory, and therapeutic properties. Examples of alkaloids include morphine, quinine, nicotine, and caffeine.

Pharmacology is the branch of medicine and biology concerned with the study of drugs, their actions, and their uses. It involves understanding how drugs interact with biological systems to produce desired effects, as well as any adverse or unwanted effects. This includes studying the absorption, distribution, metabolism, and excretion of drugs (often referred to as ADME), the receptors and biochemical pathways that drugs affect, and the therapeutic benefits and risks of drug use. Pharmacologists may also be involved in the development and testing of new medications.

The ventromedial hypothalamic nucleus (VMN) is a collection of neurons located in the ventromedial region of the hypothalamus, a part of the brain that regulates various autonomic and endocrine functions. The VMN plays an essential role in regulating several physiological processes, including feeding behavior, energy balance, and glucose homeostasis. It contains neurons that are sensitive to changes in nutrient status, such as leptin and insulin levels, and helps to integrate this information with other signals to modulate food intake and energy expenditure. Additionally, the VMN has been implicated in the regulation of various emotional and motivational states, including anxiety, fear, and reward processing.

Tetrodotoxin (TTX) is a potent neurotoxin that is primarily found in certain species of pufferfish, blue-ringed octopuses, and other marine animals. It blocks voltage-gated sodium channels in nerve cell membranes, leading to muscle paralysis and potentially respiratory failure. TTX has no known antidote, and medical treatment focuses on supportive care for symptoms. Exposure can occur through ingestion, inhalation, or skin absorption, depending on the route of toxicity.

Anti-arrhythmia agents are a class of medications used to treat abnormal heart rhythms or arrhythmias. These drugs work by modifying the electrical activity of the heart to restore and maintain a normal heart rhythm. There are several types of anti-arrhythmia agents, including:

1. Sodium channel blockers: These drugs slow down the conduction of electrical signals in the heart, which helps to reduce rapid or irregular heartbeats. Examples include flecainide, propafenone, and quinidine.
2. Beta-blockers: These medications work by blocking the effects of adrenaline on the heart, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include metoprolol, atenolol, and esmolol.
3. Calcium channel blockers: These drugs block the entry of calcium into heart muscle cells, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include verapamil and diltiazem.
4. Potassium channel blockers: These medications work by prolonging the duration of the heart's electrical cycle, which helps to prevent abnormal rhythms. Examples include amiodarone and sotalol.
5. Digoxin: This drug increases the force of heart contractions and slows down the heart rate, which can help to restore a normal rhythm in certain types of arrhythmias.

It's important to note that anti-arrhythmia agents can have significant side effects and should only be prescribed by a healthcare professional who has experience in managing arrhythmias. Close monitoring is necessary to ensure the medication is working effectively and not causing any adverse effects.

Chinese herbal drugs, also known as traditional Chinese medicine (TCM), refer to a system of medicine that has been practiced in China for thousands of years. It is based on the belief that the body's vital energy, called Qi, must be balanced and flowing freely for good health. TCM uses various techniques such as herbal therapy, acupuncture, dietary therapy, and exercise to restore balance and promote healing.

Chinese herbal drugs are usually prescribed in the form of teas, powders, pills, or tinctures and may contain one or a combination of herbs. The herbs used in Chinese medicine are typically derived from plants, minerals, or animal products. Some commonly used Chinese herbs include ginseng, astragalus, licorice root, and cinnamon bark.

It is important to note that the use of Chinese herbal drugs should be under the guidance of a qualified practitioner, as some herbs can interact with prescription medications or have side effects. Additionally, the quality and safety of Chinese herbal products can vary widely depending on the source and manufacturing process.

Aconitine is a C19-norditerpenoid, based on its presence of this C18 carbon. It is barely soluble in water, but very soluble in ... If aconitine is heated in its dry state, it undergoes a pyrolysis to form pyroaconitine ((1α,3α,6α,14α,16β)-20-ethyl-3,13- ... The binding of aconitine to the channel also leads to the channel to change conformation from the inactive state to the active ... Aconitine is also soluble in mixtures of alcohol and water if the concentration of alcohol is high enough. Like many other ...
Additional Names: Mild aconitine. Literature References: Highly toxic mixture of amorphous alkaloids from Aconitum napellus L ... Ranunculaceae. Contains aconitine, mesaconitine, hypaconitine, neopelline, l-ephedrine, sparteine, neoline and napelline. Ref: ...
tag:blogger.com,1999:blog-37623912.post6686224928484459516.. ...
Kampff, W. (1954) [on acute fatal aconitine poisoning]. [Publication] Full text not available from this repository. Item Type: ...
Frketic, J. (1956) [ case of medical poisoning with aconitine]. [Publication] Full text not available from this repository. ...
Aconitine / analogs & derivatives* * Aconitine / pharmacology * Animals * Conditioning, Operant / drug effects * Dihydro-beta- ...
The left jugular vein was cannulated with PE-50 polyethylene tubing for the administration of aconitine. Aconitine (10 μg/mL) ... Sensitivity to aconitine. Eighteen hours after O3 exposure, both low- and high-O3 exposure significantly reduced the total dose ... Aconitine challenge. Eighteen hours after exposure to O3, a separate cohort of animals were anesthetized with urethane (1.5 g/ ... However, both 0.2 and 0.8 ppm O3 increased sensitivity to aconitine-induced arrhythmia formation, suggesting a latent O3- ...
Aconitine-containing Chinese herbal medicine compounds have been used to treat chronic pain syndromes and unfortunately have ... Aconitum species (ie, monkshood or wolfsbane) contain aconitine; Veratrum species contain Veratrum alkaloids. These toxins open ...
Antiarrhythmic effects of berberine on aconitine-induced ventricular and supraventricular arrhythmias. Clinical Research 1983; ...
MeSH Terms: Aconitine/analogs & derivatives; Aconitine/pharmacology; Animals; Behavior, Animal/drug effects; Dihydro-beta- ...
ACONITINE,Z,,,1,0,2,,, 2153,2872,Spherocytosis,b,2354,,1,0,2,,, 2154,11835,Rectal Tube,O,,RECTUM;RECTAL,1,0,2,,, 2155,10481, ...
Identification of aconitine, jesaconitine, hypaconitine, and mesaconitine in a forensic autopsy sample by LC-QTOF-MS/MS. XICs ( ... In all samples, aconitine, jesaconitine, hypaconitine, and mesaconitine were identified, and Fig. 4 shows representative ... left panels), TOF-MS spectra (100-1000 Da, middle panels), and TOF-MS/MS spectra (50-1000 Da, right panels) of a aconitine, b ... batrachotoxin and aconitine from Latoxan (Valence, France); phalloidin and α-amanitin from Merck Millipore (Billerica, MA, USA ...
1882: George Henry Lamson, aconitine poisoner - 2011. *2010: Zheng Minsheng, child-stabbing doctor - 2010 ...
Aconitine-containing agent enhances antitumor activity of dichloroacetate against Ehrlich carcinoma.. Pyaskovskaya ON; Boychuk ...
Cheng, P.; Lan, W.; Yan-Hong, W.; Yun-Xia, L.; Yuan, P.; Yuan, P. The toxicity of aconitine, emodin on ICC cell and the ...
Then aconitine (25 g/kg, IV)bolus has been delivered). The black column indicates the duration of the arrhythmia observation. A ... 3. In Protocol II, after stabilization, aconitine (1 M) was infused first, then vehicle, or each dose of KBR or SEA was further ... In-Vivo: Chemically induced arrhythmia: Aconitine antagonism, Digoxin-induced arrhythmia, Strophanthin/ouabain-induced ... on aconitine-induced arrhythmias in guinea pigs in vivo, in vitro, and in computer simulation studies. Journal of Pharmacology ...
Aconitine Test*. Pass. *These tests are performed on herbs when applicable.. "Seed to Shelf" Consciousness, promoted by Dr. ...
Constit. 0.4-0.8% aconitine; aconine; napelline (isoaconitine, pseudoaconitine); picraconitine; aconitic acid; itaconic acid; ...
... including a notable study on the focal application of aconitine that revitalized the argument for multiple centers of local ...
One of the dangerous plants cultivated here is monkshood, or wolfs bane, which contains aconitine, a neurotoxin and cardio ...
The limits of detection (signal-to-noise ratio of 3) were 2.64, 1.58 and 2.75 ng for aconitine, mesaconitine and hypaconitine, ... were developed for the simultaneous quantitative determination of aconitine, mesaconitine and hypaconitine in rat plasma and ...
Effect of aconitine on the metabolism of animal tissues in vitro II. Changes in the metabolism of brain, liver and kidney ... Effect of aconitine on the metabolism of brain tissue. 1954, Vol. 19, Issue 3, pp. 586-593 [Abstract] ... tissue in the presence of aconitine, potassium ions, and 2,4-dinitrophenol. 1956, Vol. 21, Issue 6, pp. 1614-1623 [Abstract] ...
Aconitine. Newb, Female. Messages:. 0. Likes Received:. 0. Trophy Points:. 0. * Adoreabull. Newb ...
Aconitine (substance). Code System Preferred Concept Name. Aconitine (substance). Concept Status. Published. ...
  • Like many other alkaloids, the basic nitrogen atom in one of the six-membered ring structure of aconitine can easily form salts and ions, giving it affinity for both polar and lipophilic structures (such as cell membranes and receptors) and making it possible for the molecule to pass the blood-brain barrier. (wikipedia.org)
  • The roots of the plant are the source of most of the alkaloids obtained from the plant such as aconitine, atisine, heterophyllin, heterophyllisin etc. (planetayurveda.com)
  • Aconite contains alkaloids like aconine, aconitine, napelline and picraconitine. (spicesmedicinalherbs.com)
  • Many herbal medicines and compositions are clinically effective but challenged by its safety risks, i.e., aconitine (AC) from aconite species. (springer.com)
  • Injection of GP-AC nanoparticles and the mixed licorice-aconite decoction, respectively, caused mild recoverable toxic effects and no death, while the aconitine, particle-free GP-AC mixture and aconite decoction induced sever toxic effects and 100 % death. (springer.com)
  • Aconitine (AC), known as devil's helmet, is a highly poisonous alkaloid derived from various aconite species. (springer.com)
  • Toxicity of the NPs was tested in vivo in comparison to pure aconitine, aconite, and licorice root decoction and reported here. (springer.com)
  • Aconitine is an alkaloid toxin produced by various plant species belonging to the genus Aconitum (family Ranunculaceae), known also commonly by the names wolfsbane and monkshood. (wikipedia.org)
  • The ephedrine alkaloid-containing colloidal nanoparticles discovered in another licorice containing Chinese medicinal decoction [ 12 ] imply that licorice root proteins would hypothetically interact with aconitine to form aggregates thereafter affecting the toxicity. (springer.com)
  • According to press release from the SFDPH the toxic alkaloid aconitine was discovered in the lab tests of both patients as well as the tea samples they provided. (csomaonline.org)
  • Aconitine can interact with the voltage-dependent sodium-ion channels, which are proteins in the cell membranes of excitable tissues, such as cardiac and skeletal muscles and neurons. (wikipedia.org)
  • In neurons, aconitine increases the permeability of the membrane for sodium ions, resulting in a huge sodium influx in the axon terminal. (wikipedia.org)
  • Properties of aconitine-induced block of KDR current in NG108-15 neurons (Lin et al. (yale.edu)
  • The acetoxyl group at the c8 position can readily be replaced by a methoxy group, by heating aconitine in methanol, to produce a 8-deacetyl-8-O-methyl derivatives. (wikipedia.org)
  • Some of these words can also be considered Aconitine synonyms. (meaningin.com)
  • Recently,Prof. Feng Nianping's research team at SHUTCM published an academic papertitled Solid Lipid NanoparticlesFormulated for Transdermal Aconitine Administration and Evaluated In Vitro andIn Vivo in the Journal of Biomedical Nanotechnology (J Biomed Nano Technol. (shutcm.edu.cn)
  • But would-be murderers had no shortage of alternatives-scientists were identifying new plant toxins, including strychnine from a tree found in India, nicotine from tobacco leaves, and aconitine, derived from the monkshood plant. (elleryqueenmysterymagazine.com)
  • If aconitine is heated in its dry state, it undergoes a pyrolysis to form pyroaconitine ((1α,3α,6α,14α,16β)-20-ethyl-3,13-dihydroxy-1,6,16-trimethoxy-4-(methoxymethyl)-15-oxoaconitan-14-yl benzoate) with the chemical formula C32H43NO9. (wikipedia.org)
  • Aconitine binds to the channel at the neurotoxin binding site 2 on the alpha subunit (the same site bound by batrachotoxin, veratridine, and grayanotoxin). (wikipedia.org)
  • A sensitive, reliable and accurate high-performance liquid chromatography (HPLC) method coupled with photodiode array detector (DAD) were developed for the simultaneous quantitative determination of aconitine, mesaconitine and hypaconitine in rat plasma and urine by optimizing the extraction, separation and analytical conditions. (ajol.info)
  • The limits of detection (signal-to-noise ratio of 3) were 2.64, 1.58 and 2.75 ng for aconitine, mesaconitine and hypaconitine, respectively. (ajol.info)
  • Like many other alkaloids, the basic nitrogen atom in one of the six-membered ring structure of aconitine can easily form salts and ions, giving it affinity for both polar and lipophilic structures (such as cell membranes and receptors) and making it possible for the molecule to pass the blood-brain barrier. (wikipedia.org)
  • Aconitine binds to the channel at the neurotoxin binding site 2 on the alpha subunit (the same site bound by batrachotoxin, veratridine, and grayanotoxin). (wikipedia.org)
  • One of the dangerous plants cultivated here is monkshood, or wolf's bane, which contains aconitine, a neurotoxin and cardio toxin. (homeinsur.net)
  • A separate cohort was tested for vulnerability to aconitine-induced arrhythmia 24 hr after exposure. (nih.gov)
  • However, both 0.2 and 0.8 ppm O 3 increased sensitivity to aconitine-induced arrhythmia formation, suggesting a latent O 3 -induced alteration in myocardial excitability. (nih.gov)
  • In-Vivo: Chemically induced arrhythmia: Aconitine antagonism, Digoxin-induced arrhythmia, Strophanthin/ouabain-induced arrhythmia, Adrenaline-induced arrhythmia, and Calcium-induced arrhythmia. (nih.gov)
  • The poison aconitine is responsible for the toxicity of the plant which can harm an adult even with a touch. (wonderslist.com)
  • You can produce lots of other sicknesses with arsenic or thallium or atropine or aconitine or digitalis if you dose them carefully. (stackexchange.com)
  • If aconitine is heated in its dry state, it undergoes a pyrolysis to form pyroaconitine ((1α,3α,6α,14α,16β)-20-ethyl-3,13-dihydroxy-1,6,16-trimethoxy-4-(methoxymethyl)-15-oxoaconitan-14-yl benzoate) with the chemical formula C32H43NO9. (wikipedia.org)
  • Aconitine is also soluble in mixtures of alcohol and water if the concentration of alcohol is high enough. (wikipedia.org)
  • For pioneers of anesthesia such as China's Hua Tuo (c. 140-c. 208) and Japan's Seishu Hanaoka (1760-1835), the numbing aconitine of monkshoods provided the "pain dulling" portion of a primitive balanced anesthetic. (silverchair.com)