A long-acting calcium-blocking agent with significant anti-anginal activity. The drug produces significant coronary vasodilation and modest peripheral effects. It has antihypertensive and selective anti-arrhythmia activities and acts as a calmodulin antagonist.
A class Ib anti-arrhythmia agent used to manage ventricular and supraventricular arrhythmias.
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.
Pyrrolidines are saturated, heterocyclic organic compounds containing a five-membered ring with four carbon atoms and one nitrogen atom (NRCH2CH2), commonly found as structural components in various alkaloids and used in the synthesis of pharmaceuticals and other organic materials.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.
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.
A voltage-gated potassium channel that is expressed primarily in the HEART.
A genetically heterogeneous group of heritable disorders resulting from defects in protein N-glycosylation.
A family of voltage-gated potassium channels that are characterized by long N-terminal and C-terminal intracellular tails. They are named from the Drosophila protein whose mutation causes abnormal leg shaking under ether anesthesia. Their activation kinetics are dependent on extracellular MAGNESIUM and PROTON concentration.
A transient loss of consciousness and postural tone caused by diminished blood flow to the brain (i.e., BRAIN ISCHEMIA). Presyncope refers to the sensation of lightheadedness and loss of strength that precedes a syncopal event or accompanies an incomplete syncope. (From Adams et al., Principles of Neurology, 6th ed, pp367-9)
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.

ESR study on the structure-antioxidant activity relationship of tea catechins and their epimers. (1/127)

The purpose of this study is to examine the relationship between the free radical scavenging activities and the chemical structures of tea catechins ((-)-epigallocatechin gallate (EGCG), (-)-epigallocatechin (EGC) and (-)-epicatechin (EC)) and their corresponding epimers ((-)-gallocatechin gallate (GCG), (-)-gallocatechin (GC) and (+)-catechin ((+)-C)). With electron spin resonance (ESR) we investigated their scavenging effects on superoxide anions (O-.2) generated in the irradiated riboflavin system, singlet oxygen(1O2) generated in the photoradiation-hemoporphyrin system, the free radicals generated from 2,2'-azobis(2-amidinopropane)hydrochloride (AAPH) and 1, 1-diphenyl-2-picrylhydrazyl (DPPH) radical. The results showed that the scavenging effects of galloylated catechins (EGCG and GCG) on the four free radicals were stronger than those of nongalloylated catechins (EGC, GC, EC, (+)-C), and the scavenging effects of EGC and GC were stronger than those of EC and (+)-C. Thus, it is suggested that the presence of the gallate group at the 3 position plays the most important role in their free radical-scavenging abilities and an additional insertion of the hydroxyl group at the 5' position in the B ring also contributes to their scavenging activities. Moreover, the corresponding phenoxyl radicals formed after the reaction with O-.2 were trapped by DMPO and the ESR spectra of DMPO/phenoxyl radical adducts were observed (aN=15.6 G and aHbeta=21.5 G). No significant differences were found between the scavenging effects of the catechins and their epimers when their concentrations were high. However, significant differences were observed at relatively low concentrations, and the lower their concentrations, the higher the differences. The scavenging abilities of GCG, GC and (+)-C were stronger than those of their corresponding epimers (EGCG, EGC and EC). The differences between their sterical structures played a more important role in their abilities to scavenge large free radicals, such as the free radicals generated from AAPH and the DPPH radical, than to scavenge small free radicals, such as O-.2 and 1O2, especially in the case with EGCG and GCG with more bulky steric hindrance.  (+info)

Role of Ca2+ and cross-bridges in skeletal muscle thin filament activation probed with Ca2+ sensitizers. (2/127)

Thin filament regulation of contraction is thought to involve the binding of two activating ligands: Ca2+ and strongly bound cross-bridges. The specific cross-bridge states required to promote thin filament activation have not been identified. This study examines the relationship between cross-bridge cycling and thin filament activation by comparing the results of kinetic experiments using the Ca2+ sensitizers caffeine and bepridil. In single skinned rat soleus fibers, 30 mM caffeine produced a leftward shift in the tension-pCa relation from 6.03 +/- 0.03 to 6.51 +/- 0.03 pCa units and lowered the maximum tension to 0.60 +/- 0.01 of the control tension. In addition, the rate of tension redevelopment (ktr) was decreased from 3.51 +/- 0.12 s-1 to 2.70 +/- 0.19 s-1, and Vmax decreased from 1.24 +/- 0.07 to 0.64 +/- 0.02 M.L./s. Bepridil produced a similar shift in the tension-pCa curves but had no effect on the kinetics. Thus bepridil increases the Ca2+ sensitivity through direct effects on TnC, whereas caffeine has significant effects on the cross-bridge interaction. Interestingly, caffeine also produced a significant increase in stiffness under relaxing conditions (pCa 9.0), indicating that caffeine induces some strongly bound cross-bridges, even in the absence of Ca2+. The results are interpreted in terms of a model integrating cross-bridge cycling with a three-state thin-filament activation model. Significantly, strongly bound, non-tension-producing cross-bridges were essential to modeling of complete activation of the thin filament.  (+info)

Transmembrane regulation of intracellular calcium by a plasma membrane sodium/calcium exchanger in mouse ova. (3/127)

Regulation of cytoplasmic free calcium concentration ([Ca2+)]i) is a key factor for maintenance of viability of cells, including oocytes. Indeed, during fertilization of an ovum, [Ca2+]i is known to undergo oscillations, but it is unknown how basal [Ca2+]i or calcium oscillations are regulated. In the present study we investigated the role of the plasma membrane in regulating [Ca2+]i of metaphase II-arrested mouse oocytes (ova). Ova were collected from B6C3F1 mice treated with eCG (10 IU) and hCG (5 IU), and intracellular calcium was determined by means of fura-2. Extracellular calcium flux across the zona pellucida was detected noninvasively by a calcium ion-selective, self-referencing microelectrode that was positioned by a computer-controlled micromanipulator. Under basal conditions ova exhibited a calcium net efflux of 20.6 +/- 5.2 fmol/cm2 per sec (n = 69). Treatment of ova with ethanol (7%) or thapsigargin (25 nM-2.5 microM) transiently increased intracellular calcium and stimulated calcium efflux that paralleled levels of [Ca2+]i. The presence of a Na+/Ca2+ exchanger was indicated by experiments employing both bepridil, an inhibitor of Na+/Ca2+ exchange, and sodium-depleted media. In the presence of bepridil, a net influx of calcium was revealed across the zona pellucida, which was reflected by an increase in the [Ca2+]i. In addition, replenishment of extracellular sodium to ova that had been incubated in sodium-depleted media induced a large calcium efflux, consistent with the actions of Na+/Ca2+ exchange. Sodium/calcium exchange in mouse ova may be an important mechanism that regulates [Ca2+]i.  (+info)

Fucoxanthin as the major antioxidant in Hijikia fusiformis, a common edible seaweed. (4/127)

The radical scavenging activity of Japanese edible seaweeds was screened by the DPPH (1-diphenyl-2-picrylhydrazyl) assay to evaluate the DPPH radical scavenging activity in organic extracts. The fresh brown alga Hijikia fusiformis showed the strongest DPPH radical scavenging activity, followed by Undaria pinnatifida and Sargassum fulvellum. The major active compound from Hijikia fusiformis in its acetone extract was identified as fucoxanthin by 13C-NMR spectroscopy.  (+info)

Radical scavenging activity of phenylpropanoid glycosides in Caryopteris incana. (5/127)

In our screening program for antioxidants from traditional drugs and foodstuffs, one new phenylpropanoid glycoside, incanoside, was isolated together with four known phenylpropanoid glycosides, verbascoside, isoverbascoside, phlinoside A, and 6-O-caffeoyl-beta-D-glucose from the whole plant of Caryopteris incana (Thunb.) Miq. On the basis of chemical evidence and spectral analysis data, the structure of incanoside was determined to be 1-O-(3,4-dihydroxyphenyl)ethyl-O-beta-D-glucopyranosyl (1-->2)-alpha-L-rhamnopyranosyl(1-->3)-6-O-caffeoyl-beta-D- glucopyranoside. The four phenylpropanoid glycosides exhibited potent radical scavenging activity against DPPH, hydroxyl (.OH), and superoxide anion (O2-.) radicals.  (+info)

Block of rapid depolarization induced by in vitro energy depletion of rat dorsal vagal motoneurones. (6/127)

1. The ionic mechanisms contributing to the rapid depolarization (RD) induced by in vitro ischaemia have been studied in dorsal vagal motoneurones (DVMs) of brainstem slices. Compared with CA1 hippocampal neurones, RD of DVMs was slower, generally occurred from a more depolarized membrane potential and was accompanied by smaller increases in [K+]o. 2. RD was not induced by elevation of [K+]o to values measured around DVMs during in vitro ischaemia or by a combination of raised [K+]o and 2-5 microM ouabain. 3. Neither TTX (5-10 microM) nor TTX combined with bepridil (10-30 microM), a Na+-Ca2+ exchange inhibitor, slowed RD. Block of voltage-dependent Ca2+ channels with Cd2+ (0.2 mM) and Ni2+ (0.3 mM) led to an earlier onset of RD, possibly because [K+]o was higher than that measured during in vitro ischaemia in the absence of divalent ions. 4. When [Na+]o was reduced to 11.25-25 mM, RD did not occur, although a slow depolarization was observed. RD was slowed (i) by 10 mM Mg2+ and 0.5 mM Ca2+, (ii) by a combination of TTX (1.5-5 microM), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and D-2-amino-5-phosphonovalerate (AP5, 50 microM) and (iii) by TTX (1.5-5 microM) and AP5 (50 microM). 5. Ni2+ at concentrations of 0.6 or 1.33 mM blocked RD whereas 0.6 mM Cd2+ did not. A combination of Cd2+ (0.2 mM), Ni2+ (0.3 mM), AP5 (50 microM) and bepridil (10 microM) was largely able to mimic the effects of high concentrations of Ni2+. 6. It is concluded that RD is due to Na+ entry, predominantly through N-methyl-D-aspartate receptor ionophores, and to Ca2+ entry through voltage-dependent Ca2+ channels. These results are consistent with known changes in the concentrations of extracellular ions when ischaemia-induced rapid depolarization occurs.  (+info)

Pharmacological inhibition of the Na(+)/Ca(2+) exchanger enhances depolarizations induced by oxygen/glucose deprivation but not responses to excitatory amino acids in rat striatal neurons. (7/127)

BACKGROUND AND PURPOSE: Neuronal Na(+)/Ca(2+) exchanger plays a relevant role in maintaining intracellular Ca(2+) and Na(+) levels under physiological and pathological conditions. However, the role of this exchanger in excitotoxicity and ischemia-induced neuronal injury is still controversial and has never been studied in the same neuronal subtypes. METHODS: We investigated the effects of bepridil and 3',4'-dichlorobenzamil (DCB), 2 blockers of the Na(+)/Ca(2+) exchanger, in rat striatal spiny neurons by utilizing intracellular recordings in brain slice preparations to compare the action of these drugs on the membrane potential changes induced either by oxygen and glucose deprivation (OGD) or by excitatory amino acids (EAAs). RESULTS: Bepridil (3 to 100 micromol/L) and DCB (3 to 100 micromol/L) caused a dose-dependent enhancement of the OGD-induced depolarization measured in striatal neurons. The EC(50) values for these effects were 31 micromol/L and 29 micromol/L, respectively. At these concentrations neither bepridil nor DCB altered the resting membrane properties of the recorded cells (membrane potential, input resistance, and current-voltage relationship). The effects of bepridil and DCB on the OGD-induced membrane depolarization persisted in the presence of D-2-amino-5-phosphonovalerate (50 micromol/L) plus 6-cyano-7-nitroquinoxaline-2,3-dione (20 micromol/L), which suggests that they were not mediated by an enhanced release of EAAs. Neither tetrodotoxin (1 micromol/L) nor nifedipine (10 micromol/L) affect the actions of these 2 blockers of the Na(+)/Ca(2+) exchanger, which indicates that voltage-dependent Na(+) channels and L-type Ca(2+) channels were not involved in the enhancement of the OGD-induced depolarization. Conversely, the OGD-induced membrane depolarization was not altered by 5-(N, N-hexamethylene) amiloride (1 to 3 micromol/L), an inhibitor of the Na(+)/H(+) exchanger, which suggests that this antiporter did not play a prominent role in the OGD-induced membrane depolarization recorded from striatal neurons. Bepridil (3 to 100 micromol/L) and DCB (3 to 100 micromol/L) did not modify the amplitude of the excitatory postsynaptic potentials evoked by cortical stimulation. Moreover, these blockers did not affect membrane depolarizations caused by brief applications of glutamate (0.3 to 1 mmol/L), AMPA (0. 3 to 1 micromol/L), and NMDA (10 to 30 micromol/L). CONCLUSIONS: These results provide pharmacological evidence that the activation of the Na(+)/Ca(2+) exchanger exerts a protective role during the early phase of OGD in striatal neurons, although it does not shape the amplitude and the duration of the electrophysiological responses of these cells to EAA.  (+info)

p-Chlorobenzyltetrahydroberberine inhibits vascular smooth muscle contractions caused by Ca2+. (8/127)

AIM: To investigate influences of p-chlorobenzyltetrahydroberberine (CPU-86017) and levothyroxin (Lev) on vascular smooth muscle (VSM) contractions by intracellular Ca2+ release and calcium entry. METHODS: Three kinds of contractions of rat thoracic aortic rings were used to compare suppression by CPU-86017, bepridil (Bep), verapamil (Ver), and nimodipine (Nim) in euthyroid- and Lev-induced hyperthyroidism rats. RESULTS: The IC50 of CPU-86017 on KCl-induced contractions of euthyroid and hyperthyroid VSM were 80 (36-179) and 121 (62-236) mumol.L-1, respectively. The potency of CPU-86017 was approximate to 1/10 of Bep and 1/100 of Ver and Nim. Suppressions of Ver and Nim on hyperthyroid VSM in Ca(2+)-free solution were greatly attenuated by -86% and -95%, respectively. Slight or no change in activity of CPU-86017 and Bep was found. Contractions on adding Ca2+ into Ca(2+)-free medium were suppressed by CPU-86017 and its potencies in euthyroid and hyperthyroid rats were not different. CONCLUSION: CPU-86017 is more potent to suppress Ca2+ entry than intracellular calcium mobilization and Lev enhances both.  (+info)

Bepridil is a calcium channel blocker medication that is used to treat angina (chest pain) and certain types of irregular heart rhythms. It works by relaxing the blood vessels and increasing the supply of oxygen and blood to the heart.

Here is the medical definition of Bepridil:

Bepridil is a non-dihydropyridine calcium channel blocker that selectively inhibits the L-type calcium channels in cardiac and smooth muscle cells, resulting in vasodilation, negative inotropic and chronotropic effects on the heart. It is used in the management of chronic stable angina pectoris and certain types of arrhythmias. The most common side effects include dizziness, headache, nausea, and constipation. Bepridil has a negative inotropic effect and should be used with caution in patients with heart failure or reduced left ventricular function. It is also metabolized by the cytochrome P450 system and can interact with other medications that are metabolized by this pathway.

Aprindine is a class IA antiarrhythmic agent, which is primarily used to treat cardiac arrhythmias (abnormal heart rhythms). It works by blocking sodium channels in the heart muscle cells, which helps to stabilize the heart's electrical activity and restore normal rhythm.

The medical definition of Aprindine can be stated as:

"Aprindine is a sodium channel blocker that is used in the treatment of cardiac arrhythmias, including atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia. It works by slowing down the conduction of electrical impulses through the heart muscle cells, which helps to restore normal rhythm."

It is important to note that Aprindine can have serious side effects, including increased risk of ventricular arrhythmias and cardiac arrest, especially when used in high doses or in patients with certain underlying medical conditions. Therefore, it should only be prescribed by a healthcare professional who has experience in managing cardiac arrhythmias.

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.

Pyrrolidines are not a medical term per se, but they are a chemical compound that can be encountered in the field of medicine and pharmacology. Pyrrolidine is an organic compound with the molecular formula (CH2)4NH. It is a cyclic secondary amine, which means it contains a nitrogen atom surrounded by four carbon atoms in a ring structure.

Pyrrolidines can be found in certain natural substances and are also synthesized for use in pharmaceuticals and research. They have been used as building blocks in the synthesis of various drugs, including some muscle relaxants, antipsychotics, and antihistamines. Additionally, pyrrolidine derivatives can be found in certain plants and fungi, where they may contribute to biological activity or toxicity.

It is important to note that while pyrrolidines themselves are not a medical condition or diagnosis, understanding their chemical properties and uses can be relevant to the study and development of medications.

Calcium channel blockers (CCBs) are a class of medications that work by inhibiting the influx of calcium ions into cardiac and smooth muscle cells. This action leads to relaxation of the muscles, particularly in the blood vessels, resulting in decreased peripheral resistance and reduced blood pressure. Calcium channel blockers also have anti-arrhythmic effects and are used in the management of various cardiovascular conditions such as hypertension, angina, and certain types of arrhythmias.

Calcium channel blockers can be further classified into two main categories based on their chemical structure: dihydropyridines (e.g., nifedipine, amlodipine) and non-dihydropyridines (e.g., verapamil, diltiazem). Dihydropyridines are more selective for vascular smooth muscle and have a greater effect on blood pressure than heart rate or conduction. Non-dihydropyridines have a more significant impact on cardiac conduction and contractility, in addition to their vasodilatory effects.

It is important to note that calcium channel blockers may interact with other medications and should be used under the guidance of a healthcare professional. Potential side effects include dizziness, headache, constipation, and peripheral edema.

Long QT syndrome (LQTS) is a cardiac electrical disorder characterized by a prolonged QT interval on the electrocardiogram (ECG), which can potentially trigger rapid, chaotic heartbeats known as ventricular tachyarrhythmias, such as torsades de pointes. These arrhythmias can be life-threatening and lead to syncope (fainting) or sudden cardiac death. LQTS is often congenital but may also be acquired due to certain medications, medical conditions, or electrolyte imbalances. It's essential to identify and manage LQTS promptly to reduce the risk of severe complications.

Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.

During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.

ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.

The KCNQ1 potassium channel, also known as the Kv7.1 channel, is a voltage-gated potassium ion channel that plays a crucial role in the regulation of electrical excitability in cardiac myocytes and inner ear epithelial cells. In the heart, it helps to control the duration and frequency of action potentials, thereby contributing to the maintenance of normal cardiac rhythm. Mutations in the KCNQ1 gene can lead to various cardiac disorders, such as long QT syndrome type 1 and familial atrial fibrillation. In the inner ear, it helps regulate potassium homeostasis and is essential for hearing and balance functions. Dysfunction of this channel has been linked to deafness and balance disorders.

Congenital Disorders of Glycosylation (CDG) are a group of genetic disorders that affect the body's ability to add sugar molecules (glycans) to proteins and lipids. This process, known as glycosylation, is essential for the proper functioning of many cellular processes, including protein folding, trafficking, and signaling.

CDG can be caused by mutations in genes that are involved in the synthesis or transport of glycans. These genetic defects can lead to abnormal glycosylation patterns, which can result in a wide range of clinical manifestations, including developmental delay, intellectual disability, seizures, movement disorders, hypotonia, coagulation abnormalities, and multi-organ involvement.

CDG are typically classified into two main types: type I CDG, which involves defects in the synthesis of the lipid-linked oligosaccharide precursor used for N-glycosylation, and type II CDG, which involves defects in the processing and transfer of glycans to proteins.

The diagnosis of CDG is often based on clinical features, laboratory tests, and genetic analysis. Treatment is typically supportive and multidisciplinary, focusing on addressing specific symptoms and improving quality of life. In some cases, dietary modifications or supplementation with mannose or other sugars may be beneficial.

Ether-à-go-go (EAG) potassium channels are a type of voltage-gated potassium channel that are widely expressed in the heart, brain, and other tissues. They are named after the ethereal dance movements observed in fruit flies with mutations in these channels.

EAG potassium channels play important roles in regulating electrical excitability and signaling in excitable cells. In the heart, they help to control the duration of the action potential and the refractory period, which is critical for maintaining normal heart rhythm. In the brain, they are involved in regulating neuronal excitability and neurotransmitter release.

Mutations in EAG potassium channels have been associated with various human diseases, including cardiac arrhythmias, epilepsy, and bipolar disorder. The medical definition of "Ether-A-Go-Go Potassium Channels" refers to the genetic components that make up these channels and their role in physiological processes and disease states.

Syncope is a medical term defined as a transient, temporary loss of consciousness and postural tone due to reduced blood flow to the brain. It's often caused by a drop in blood pressure, which can be brought on by various factors such as dehydration, emotional stress, prolonged standing, or certain medical conditions like heart diseases, arrhythmias, or neurological disorders.

During a syncope episode, an individual may experience warning signs such as lightheadedness, dizziness, blurred vision, or nausea before losing consciousness. These episodes usually last only a few minutes and are followed by a rapid, full recovery. However, if left untreated or undiagnosed, recurrent syncope can lead to severe injuries from falls or even life-threatening conditions related to the underlying cause.

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.

... (trade name Vascor) is an diamine calcium channel blocker once used to treat angina pectoris. It is no longer sold in ... March 2021). "Bepridil is potent against SARS-CoV-2 in vitro". Proceedings of the National Academy of Sciences of the United ... A research paper showed that Bepridil inhibited cytopathogenic effects induced by SARS-CoV-2 in Vero E6 cells and in A549 cells ... May 2008). "Use of bepridil in combination with Ic antiarrhythmic agent in converting persistent atrial fibrillation to sinus ...
It is found in many drugs such as procyclidine and bepridil. It also forms the basis for the racetam compounds (e.g. piracetam ...
These include mibefradil, bepridil, flunarizine (BBB crossing), fluspirilene (BBB crossing), and fendiline. Gabapentinoids, ...
"Intracellular Ca2+ mediates the cytotoxicity induced by bepridil and benzamil in human brain tumor cells". Cancer Letters. 88 ( ...
A number of compounds can also bind to cCTnC with low affinity: EMD 57033, resveratrol, bepridil, and EGCG. All of these ... Li Y, Love ML, Putkey JA, Cohen C (May 2000). "Bepridil opens the regulatory N-terminal lobe of cardiac troponin C". ... and bepridil. The calmodulin antagonist, W7, has also been found to bind to cNTnC to act as a troponin inhibitor. All of these ... "Structure of the regulatory N-domain of human cardiac troponin C in complex with human cardiac troponin I147-163 and bepridil ...
Thus, interactions are to be expected with known P-glycoprotein inhibitors such as amiodarone, bepridil, diltiazem, ciclosporin ...
... bepridil MeSH D03.383.773.165 - clemastine MeSH D03.383.773.170 - 3,4-dichloro-n-methyl-n-(2-(1-pyrrolidinyl)-cyclohexyl)- ...
... bepridil, IV erythromycin, halofantrine, pentamidine, sultopride, terfenadine, and vincamine). Symptoms of over dosage would be ...
Alverine Amiodarone Amitriptyline Amlodipine Aprindine Astemizole AY-9944 Benzatropine Bepridil Biperiden Camylofin Carvedilol ...
Ethioninie Suloctidil Terodiline Bepridil Gamma-Hydroxybutyric acid or "GHB" is a GABA analogue that is a natural occurring ...
Bepridil (INN) Beraprost (INN) Berefrine (INN) Berlafenone (INN) Bermoprofen (INN) Berocca PN Beroctocog alfa (INN) Berotec ...
... combinations C08DB01 Diltiazem C08EA01 Fendiline C08EA02 Bepridil C08EX01 Lidoflazine C08EX02 Perhexiline C08GA01 Nifedipine ...
Bepridil (trade name Vascor) is an diamine calcium channel blocker once used to treat angina pectoris. It is no longer sold in ... March 2021). "Bepridil is potent against SARS-CoV-2 in vitro". Proceedings of the National Academy of Sciences of the United ... A research paper showed that Bepridil inhibited cytopathogenic effects induced by SARS-CoV-2 in Vero E6 cells and in A549 cells ... May 2008). "Use of bepridil in combination with Ic antiarrhythmic agent in converting persistent atrial fibrillation to sinus ...
Bepridil (Vascor) Diltiazem (Cardizem, Dilacor, Tiazac) Felodipine (Plendil) Isradipine (Dyna Circ) Norvasc (Amlodipine) ...
... bepridil (Vascor); cannabinoids such as dronabinol (Marinol), nabilone (Cesamet) or marijuana (cannabis); digoxin (Lanoxin); ...
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Check with your doctor right away if you have pain or tenderness in the upper stomach, pale stools, dark urine, loss of appetite, nausea, vomiting, unusual tiredness or weakness, or yellow eyes or skin. These could be symptoms of a serious liver problem. This medicine may cause serious lung or breathing problems (eg, interstitial lung disease, pneumonitis). Check with your doctor right away if you have chest pain, chills, cough, fever, general feeling of discomfort or illness, thickening of bronchial secretions, or trouble breathing. Check with your doctor right away if blurred vision, dizziness, nervousness, headache, pounding in the ears, or slow or fast heartbeat occurs during or after treatment with this medicine. These can be symptoms of hypertension (high blood pressure). This medicine can cause changes in your heart rhythm, including a condition called QT prolongation. Call your doctor right away if you have dizziness, fainting, or slow, fast, pounding, or uneven heartbeats. This medicine ...
Detailed drug Information for Duo-Vil 2-25. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Detailed drug Information for Toremifene. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
This medicine comes with a patient information insert. Read and follow these instructions carefully. Ask your doctor or pharmacist if you have any questions. The solution comes in small containers that are only used one time. Throw the empty container away after putting the medicine into your ear(s). This medicine should be used only inside the ear. Do not put it in the eyes or nose, and do not take it by mouth. If this medicine is swallowed by accident or gets into your eyes, call your doctor right away. It is important that the infected ear remain clean and dry. When bathing, avoid getting the infected ear wet. Avoid swimming unless your doctor has instructed you otherwise. To use the ear drops:. ...
Torsade de pointes is an uncommon and distinctive form of polymorphic ventricular tachycardia (VT) characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line (see the image below). Torsade de pointes, often referred to as torsade, is associated with a prolonged QT interval, which may be co...
... bepridil, sparfloxacin, and terodiline. (The preceding lists of drugs are not comprehensive.) ... bepridil, sparfloxacin, and terodiline. The preceding lists of drugs are not comprehensive. ... bepridil, sparfloxacin, and terodiline. The preceding lists of drugs are not comprehensive. ...
Bepridil is a commonly used medication for arrhythmia and heart failure. It primarily exerts hemodynamic effects by inhibiting ...
Bepridil.. The next group should alert you because it can cause severe side effects or even fatal consequences. They are ...
Cardiac medications (eg, quinidine, procainamide, disopyramide, sotalol, probucol, bepridil, dofetilide, ibutilide) * ...
... bepridil hydrochloride, encainide hydrochloride, flecainide acetate, propafenone, or quinidine); ergot alkaloid derivatives; ...
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Bepridil (INN). D00631 Bepridil hydrochloride (USAN); Bepridil hydrochloride hydrate (JAN) ,JP,. DG00334 ...
Such drugs include many antiarrhythmics, some phenothiazines, bepridil, tricyclic antidepressants, and certain oral macrolides ... bepridil, tricyclic antidepressants and oral macrolides (see WARNINGS and Use with Drugs that Prolong QT Interval and ...
Cardiovascular QT prolonging medicinal products (e.g. quinidine, disopyramide, bepridil, sotalol, ibutilide, amiodarone). ...
medicines that may affect the function of the heart such as chloroquine, halofantrine, haloperidol, methadone, bepridil ...
... bepridil hydrochloride, encainide hydrochloride, flecainide acetate, propafenone, or quinidine); ergot alkaloid derivatives; ...
Bepridil, cisaprida, difemanil, eritromicina IV, halofantrina, mizolastina, pentamidina, esparfloxacino, terfenadina, vincamina ...
... bepridil, fendiline, lidoflazine and perhexiline; ATC codes=C08E) and vascular selective CCBs (all other CCBs; ATC codes=C08C ...
... diltiazem and bepridil ... Verapamil, bepridil and diltiazem have promi- nent cardiac ...
Drug-Drug Interactions: CALMBETA 20 TABLET 10S may interact with antacid (aluminium hydroxide), anti-arrhythmic (bepridil), ...
... and bepridil as somewhat less potent. ...
They focussed on four drugs: benztropine, bepridil, paroxetine and sertraline, which they noted could all bind to the same ...
... which normalized after the cessation of bepridil. This case report suggests that a history of drug-induced QT prolongation can ...
"In vitro and experimental therapeutic studies of the calcium channel blocker bepridil: detection of viable Leishmania (L.) ...
  • Combining fluconazole with amiodarone Cordarone pimozide Orap bepridil Vascor or other drugs that affect heart rhythm may increase the risk of abnormal heart rhythms. (njacs.org)
  • Bepridil (trade name Vascor) is an diamine calcium channel blocker once used to treat angina pectoris. (wikipedia.org)
  • The relative potency of CCBs as vasodilators varies, with dihydropyridine-type compounds, such as nifedipine, regarded as the most potent subclass, and verapamil, diltiazem, and bepridil as somewhat less potent. (medscape.com)
  • They focussed on four drugs: benztropine, bepridil, paroxetine and sertraline, which they noted could all bind to the same large cavity within the glycoprotein. (diamond.ac.uk)
  • CALMBETA 20 TABLET 10'S may interact with antacid (aluminium hydroxide), anti-arrhythmic (bepridil), anti-cholinergic (atropine), anti-psychotic (chlorpromazine), anti-convulsant (carbamazepine), barbiturates, and anti-anxiety drugs. (apollopharmacy.in)
  • A research paper showed that Bepridil inhibited cytopathogenic effects induced by SARS-CoV-2 in Vero E6 cells and in A549 cells in an in vitro assay. (wikipedia.org)
  • Bepridil is a commonly used medication for arrhythmia and heart failure. (tcdb.org)
  • The pilot intervention systemic or ophthalmic 2 highly endemic oral dosage forms with oral bepridil, a result of ago I had Unguja resident population no serious negative provides tools for healing, respectively. (grey-panthers.it)
  • Non-selective inhibitors include the inorganic cations nickel and cadmium and compounds such as amiloride bepridil and amiodarone. (healthyconnectionsinc.com)
  • The calcium antagonist drugs bepridil, nitrendipine, fendilene, nifedipine and verapamil have all been found to have various beneficial effects in in vitro studies. (who.int)
  • The haemodynamic effects of 4 calcium antagonists, bepridil (1.25 to 5 mg/kg i.v.), diltiazem (0.1 to 0.3 mg/kg i.v.), nifedipine (0.01 to 0.03 mg/kg i.v.) and verapamil (0.1 to 0.3 mg/kg i.v.) were compared in anaesthetized open-chest dogs. (eurekamag.com)
  • Two new vascular smooth muscle relaxants, bepridil and cetiedil, were found to possess specific CaM-inhibitory properties which resembled those of trifluoperazine. (jhu.edu)
  • To this end, the scientists came to this recognition through extensive genetic analysis by means of Next Generation Sequencing (NGS) and by demonstrating a prevention of the aforementioned vascular damage by treatment with the FoxO3 activator Bepridil. (elheraldolatino.blog)
  • The study found bepridil to offer the most potential for treatment of COVID-19. (tamu.edu)
  • A research paper showed that Bepridil inhibited cytopathogenic effects induced by SARS-CoV-2 in Vero E6 cells and in A549 cells in an in vitro assay. (wikipedia.org)
  • The most marked negative chronotropic effects were seen with diltiazem, verapamil and bepridil in that order. (eurekamag.com)
  • 15. Bepridil exhibits anti-leukemic activity associated with NOTCH1 pathway inhibition in chronic lymphocytic leukemia. (nih.gov)

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