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Metabolic pathway

[edit]

Bibliography of references

[edit]
  1. Fundamentals of Biochemistry.[1]
  2. Major Metabolic Pathways and Hormone Production in Unstimulated Monolayer Cultures of the Rat Anterior Pituitary.[2]
  3. Metabolic Pathways of Glycerol Dissimilation.[3]
  4. The Quarterly Review of Biology.[4]
  5. Molecular Biology: Principles and Practice.[5]
  6. Life: The Science of Biology.[6]
  7. Organic Chemistry.[7]
  8. Ultrastructural Pathology: An Introduction to Interpretation.[8]
  9. The Physiology and Biochemistry of Prokaryotes.[9]
  10. Regulation of Primary Metabolic Pathways in Plants.[10]

Articles edited

[edit]
  1. Metabolic pathway [11]
  2. Heart failure medications
  3. Amiodarone
  4. Procainamide
  5. Ranolazine
  6. Metoprolol

See also

[edit]


Articles reviewed

[edit]
  1. Chemical specificity
  2. Protein aggregation

Metabolic pathway

[edit]
  • Different metabolic pathways function based on the position within a eukaryotic cell and the significance of the pathway in the given compartment of the cell. For instance, the citric acid cycle, electron transport chain, and oxidative phosphorylation all take place in the mitochondrial membrane. In contrast, glycolysis, pentose phosphate pathway, and fatty acid biosynthesis all occur in the cytosol of a cell.


List of Potential Articles

[edit]
  1. Metabolic pathway [11]
  2. Rhodopsin
  3. Enzyme catalysis
  4. Redox reaction
  5. ATP synthase
  6. Biological membrane
  7. Phospholipid


Google Scholar


Table summarizing the drugs under the Vaughan Williams classifications that are frequently used in the treatment of cardiac dysrhythmias:

Drugs Used for Treatment of Heart Failure
Vaughan Williams Classification Drug Name and Approval Date Indications for Drug Use Mechanism of Action (MOA) Animal Model
Class Ia Procainamide Hydrochloride (Procanbid extended-release tablets)

Approved January 1996 (Warner-Lambert)

  • Ventricular ectopy and tachycardia, atrial fibrillation, and re-entrant and automatic supraventricular tachycardia[12]
  • Drawbacks of the Drug:
    • Causes gastrointestinal disturbances, lupus syndrome, ventricular tachydysrhythmias, and aggravates pre-existing abnormalities in impulse initiation and propagation[12]
    • Initiates leukopenia and/or agranulocytosis, which are serious hematologic disorders
    • Prolongs QT interval of action potential and increases the risk of torsade de points[13]
  • Prolongs refractoriness of the atria, AV node, and the His-Purkinje fibers, and prolongs the HV intervals of the His-Purkinje System[12]
  • Increases concentration-depedent action potential duration, refractory period, and the diastolic threshold potential[14]
  • In addition to blocking the INa current (Na+ channel blocker), it inhibits the IKr rectifier K+ current[13]
  • Induces a voltage-dependent open channel block on the batrachotoxin (BTX)-activated sodium channels in cardiomyocytes[15]
  • Ventricular tachycardia induced through the left anterior descending coronary artery in dogs (proximal occlusion ligation)
  • Ectopic tachycardia induced by chloroform-adrenaline in cats[16]
  • Perfused hearts of guinea-pigs and rabbits[13]
Class Ib Ranolazine (Ranexa)

Initial U.S. Approval in 2006 for oral use as an antianginal agent

Antiarrhythmic properties are also observed, yet is not approved for atrial or ventricular fibrillation in the U.S.

  • Chronic angina and ventricular fibrillation (VFib has not been approved yet, but multiple research articles support its effects[17][18][19]
  • Prolongs action potential duration, with corresponding QT interval prolongation on electrocardiography
  • Blocks the INa current and prevents calcium overload caused by the hyperactive INa current, thus it stabilizes the membrane and reducing excitability[19]
  • Exhibits its effects on the delayed rectifier current (hERG/IKr Potassium channels), inhibits the late inward Na+ current (INa), moderate inhibitor for CYP3A and P-gp (cyclosporine), stimulates myogenesis, reduces a pro-oxidant inflammation/oxidative condition, and activates the calcium signaling pathway[20]
  • Ventricular fibrillation in an isolated rabbit heart under hypoxia and reoxygenation conditions and in the presence of pinacidil, which is an ATP-dependent potassium channel opener[17]
  • Ventricular and atrial fibrillation were studied in Yorkshire pigs preanesthetized with telaol and xylazine and anesthetized with alpha-chloralose - the catheter was placed in the right atrium through the femoral vein for AFib and in the left ventricle via the left carotid artery for VFib[18]
Class Ic Propafenone (Rythmol)

Approved January 1998 (Knoll Pharmaceutical)

  • Paroxysmal atrial fibrillation
  • Inhibits sodium channel protein type 5 subunit alpha and potassium voltage-gated channel subfamily H member 2
  • Propafenone inhibits RyR2 channels in the open state, suppresses Ca2+ waves and prevents CPVT[21]
  • In Purkinje fibers, and myocardial fibers (to a lesser extent), propafenone reduces the fast inward current carried by sodium ions, which is responsible for the drugs antiarrhythmic actions. Diastolic excitability threshold is increased and effective refractory period prolonged[22]
  • Beagle dogs of either sex were anesthetized, then the left carotid artery was isolated and a guide catheter inserted and positioned at the left coronary ostium under fluoroscopic control and infarction was induced through catheter balloon. Five or six days after myocardial infarction, animals were re-anesthetized and propafenone was administered[23]
Class II Metoprolol Succinate (Toprol-XL)

Approved January 1995 (for atrial fibrillation) (AstraZeneca)

  • Hypertension, angina pectoris, congestive heart failure, and atrial fibrillation[24]
  • Blocks ß1 adrenergic receptors of cardiomyocytes, thus it decreases the slope of phase 4 in the nodal action potential (reduces Na+ uptake) and prolongs repolarization of phase 3 (slows down K+ release)[24]
  • Suppresses the norepinephrine-induced increase in the sarcoplasmic reticulum (SR) Ca2+ leak and the spontaneous SR Ca2+ release, which are the major triggers for atrial fibrillation[24]
  • Inhibits adrenergic ß1 receptors of the pacemaker cells of the sinoatrial and atrioventricular nodes[25]
  • Atrial fibrillation induced in Yorkshire pigs and Boer goats by rapid atrial pacing (RAP) through implanted pacemakers[26]
  • Atrial fibrillation induced by trans-esophageal atrial burst pacing[24]
Class III Amiodarone Hydrochloride (Marketed as Cordarone and Pacerone)

Initial FDA Approval in 1985 for ventricular tachycardia and fibrillation as an oral tablet and in 1995 for atrial arrhythmia as an injection for intravenous use (Herendael 2010) International Medication System, Ltd., Zydus Pharmaceuticals USA Inc., Teva, Mylan, etc. (Currently on the market as a tablet for oral uptake and as an injection)

  • Reccurent ventricular fibrillation and recurrent hemodynamically unstable ventricular tachycardia, congestive heart failure, and atrial fibrillation (due to its effect on blocking the AV node, thus slowing the ventricular response rate)[27]
  • Also, it is well known to treat high grade ventricular ectopic activity (VEA), Wolff-Parkinson-White syndrome, and sick sinus syndrome[28]
  • Clinical need to suppress atrial fibrillation and an attempt to maintain the sinus rythm lead to patient trials of amiodarone administration[27]
  • Amiodarone's transition from an antianginal agent (1962–1985) to the treatment of ventricular and supraventricular tachycardias originated due to its observed antiarrhythmic properties in Europe and South America in the early 1970s[29]
  • Drawbacks of the drug: Pulmonary toxicity (hypersensitivity pneumonitis or interstitial/alveolar pneumonitis)
  • Slows conduction rate and prolongs the refractory period of the SA and AV nodes[30]
  • Prolongs the refractory periods of the ventricles, bundles of His, and the Purkinje fibres without exhibiting any effects on the conduction rate[30]
  • Prolongs the myocardial cell action potential duration and refractory period and is a non-competitive ß-adrenergic inhibitor[31]
  • Inhibits the voltage-dependent K+ and Na+ channels, and exhibits calcium channel blocking and beta-blocking effects[32]
  • In the animal models below, amiodarone was administered intravenously
  • Ventricular arrhythmias:
    • Chloroform-induced ventricular fibrillation (VFib) in mice
    • VFib induced in rats via an I.V. injection of CaCl2
    • Ventricular tachycardia (VTach) evoked in rats and dogs by aconitine hydrochloride
    • Experimental arrhythmias (known as multifocal ventricular ectopic beats) were induced by an IV injection of epinephrine in anesthetized dog, IV injection of barium chloride in anesthetized rabbit and dog, and IV injection of a large dose of strophanthin in the morphinized dog[30]
    • Experimental VTach in guinea pigs by an induction of either oubtain or isoproterenol[30]
    • VFib after coronary artery ligation in dogs and rats.
  • Supraventricular arrhythmias
    • Acetylcholine-induced atrial fibrillation (AFib) in dogs, aconite-induced AFib in cats, and electrically induced AFib in dogs[30]
    • Mongrel dogs were anaesthetized with sodium pentobarbital and atropinized. Adrenoceptor stimulation was achieved by IV administration of adrenaline and measurement of increased blood pressure via a catheter inserted into the femoral artery, Increase in heart rate was measured after an IV administration of isoprenaline[33]
Class III Dronedarone (Multaq) Approved July 2009 (for paroxysmal or persistent atrial fibrillation or atrial flutter)

(Sanofi-aventis)

  • Paroxysmal or persistent atrial fibrillation and atrial flutter
  • Advantage: Non-iodinated amiodarone derivative and is more potent than amiodarone in treating cardiac arrhythmias (atrial and ventricular)[34]
  • Illustrates antiadrenergic effects, and prolongs atrioventricular nodal conduction, atrial and ventricular refractory periods, and the duration of paced QRS interval[35]
  • Effectively blocks K+ channels, and exhibits Ca2+ and Na+ channel, and beta-blocking effects[36]
  • Ventricular fibrillation (VFib) in anesthetized pigs induced by occlusion to the left coronary descending artery[37]
  • Ventricular tachycardia (VTach) and atrial fibrillation (AFib) in Mongrel dogs anesthetized with chloralose[38]
  • Ventricular fibrillation induced by coronary artery ligation in anaesthetised rats[34]
Class III Sotalol (Betapace AF Tablet) Initial U.S. Approval in 1992 for atrial fibrillation, atrial flutter, and ventricular arrhythmias for intravenous use (FDA Drug Indications and Usage, 1)

Approved February 2000

(Berlex Laboratories)

  • Atrial fibrillation, atrial flutter, and ventricular arrhythmia[39]
  • Blocks beta-adrenoreceptors and prolongs action potential duration
  • Decreases AV nodal conduction and increases the refractory periods of atrial and ventricular myocytes[39]
  • Actively inhibits the rapid component of the delayed rectifier potassium current, IKr[40]
  • Atrial fibrillation induced by an atrial electrical remodeling of rabbits by subjecting them to rapid atrial pacing of 600 beats/min for 2–4 weeks, which led to the atrial effective refractory period[41]
Class III Ibutilide Fumarate (Corvert IV Injection) Approved December 1995 Pharmacia & Upjohn
  • Irregular contractions of the heart and Atrial Fibrillation
  • Advantage:
    • No sedation necessary, alternative to electrical cardioversion.
    • Increased AERP and prevention of induced atrial flutter
  • Drawback:
    • Can cause Torsades de Pointes
  • Activates voltage-dependent L-type calcium channel subunit alpha-1C and voltage-dependent L-type calcium channel subunit beta-1. Inhibits potassium voltage-gated channel subfamily H member 2[42]
  • Activation of a late inward sodium current and possibly blockade of the rapidly activating component of the cardiac delayed rectifier potassium current that induces prolongation of the myocardial action potential duration[43]
  • Threshold, effective refractory period, force of contraction, conduction time and rate were measured at various pacing frequencies in isolated rabbit papillary muscles, ventricular muscle strips and right atria exposed to ibutilide fumarate[44]
  • Pacing-induced sustained atrial flutter over a 7-day post-surgical period was studied in conscious dogs and alternating analysis of ibutilide (1.0 to 30.0 ug/kg) and d,l-sotalol (0.1 to 3.0 mg/kg) was determined. Ibutilide significantly increased atrial flutter cycle length (AFL CL) 11 ± 2 msec and atrial effective refractory period (AERP) 13 ± 2 msec, and terminated atrial flutter in all cases (n = 12) following a mean dose of 6 ± 2 ug/kg[45]
Class IV Verapamil; IVAX; Generic equivalent of Knoll's Isoptin SR and Searle's Calan SR, Approved December 1997
  • Supraventricular tachycardia, angina, hypertension
  • Inhibits voltage-dependent L-type calcium channel subunits 1C (1D,1F, 1S and subunits beta-1-4)[46]
  • Verapamil is a calcium ion influx inhibitor and by inhibiting the L-type calcium channel it inhibits the transmembrane influx of ionic calcium into arterial smooth muscle as well as in conductile and contractile myocardial cells. Verapamil binding is voltage-dependent with affinity increasing as the vascular smooth muscle membrane potential is reduced. In addition, verapamil binding is frequency dependent and apparent affinity increases with increased frequency of depolarizing stimulus[47]
  • Verapamil and were tested against electrically induced arrhythmias in conscious and anaesthetized rats. Stainless steel electrodes were permanently implanted; 0.3 cm apart, into the left ventricle, and fibrillo-flutter was measured in both groups. As a result, verapamil (0.2-20 mgkg-1 i.v). produced dose dependent reduction in the arrhythmias induced by coronary occlusion as judged by reduction in arrhythmia score from control values[48]
Class IV Diltiazem Hydrochloride, Extended-Release Capsules; Biovail Laboratories; Approved January 2000
  • Angina pectoris, arrhythmia, hypertension
  • Inhibits voltage-dependent L-type calcium channel gamma-1 subunit[49]
  • By diltiazem being a calcium channel blocker, it inhibits the flow of calcium ions and interferes with the slow inward (depolarizing) current in excitable tissue and causes excitation-contraction uncoupling in various myocardial tissues without changes in the configuration of the action potential[50]
  • In vivo antiarrhythmic effects of diltiazem hydrochloride on adrenaline induced ventricular arrhythmias were examined in halothane anesthetized guinea pigs. Arrhythmogenicity was significantly increased with vagotomy and higher concentration of halothane. After injection of diltiazem at 0.5 mg/kg, the arrhythmic ratio was significantly reduced compared with the pre-drug control value (0.69 vs 0.04, P<0.05). Before administration of diltiazem, the mean arrhythmogenic rate of adrenaline was 8.50 microg/kg per min, but ventricular arrhythmias were no longer induced during continuous infusion of diltiazem at 0.5 mg/kg per min[51]
  • Eight healthy horses were treated with diltiazem IV to determine the effects of diltiazem on cardiac rate and rhythm, left ventricular (LV) function, central hemodynamics, and peripheral blood flow. Cardiac effects of diltiazem included intermittent depression of the sinus and atrioventricular nodes and mild impairment of systolic and diastolic LV function. Vascular effects of diltiazem included arterial vasodilatation, increased limb blood flow, and decreased systemic vascular resistance. Because of its inhibitory effects on AV nodal conduction, diltiazem may prove useful for heart rate control in horses with AF[52]
First in Class Nesiritide (Natrecor); Scios; Approved August 2001
  • Acutely decompensated congestive heart failure
  • Particulate guanylate cyclase receptor agonist
  • Nesiritide is the recombinant form of the 32 amino acid human B-type natriuretic peptide. Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells, leading to increased intracellular concentrations of guanosine 3'5'-cyclic monophosphate (cGMP) and smooth muscle cell relaxation. (FDA Product Insert) The mechanism by which cGMP causes relaxation is unknown; however, it is shown that nitric oxide and cGMP relax vascular smooth muscle by a cGMP-dependent protein kinase-dependent activation of K channels[53]
  • In 9 healthy, chronically instrumented, conscious dogs, hemodynamic and electrophysiologic parameters were assessed at baseline and during recombinant human BNP (nesiritide) infusion at 0.03 and 0.09 microg/kg/min after 1 hour at each dose. Infusion of hBNP produced dose-related increases (P <.001) in hBNP and cyclic GMP plasma levels and reductions (P <.05) in mean arterial pressure. In conclusion, short-term infusion of recombinant hBNP has no significant effects on atrial or ventricular electrophysiologic parameters but did reduce mean arterial pressure[54]
First in Class Ivabradine (Corlanor) Approved April 2015 Amgen S16257
  • Chronic heart failure
  • Advantage:
    • Does not affect resting epicardial coronary artery diameter and only attenuated its increase during exercise
  • Drawback:
    • Blurred vision, headaches, palpitations, vertigo, shortness of breath, bradycardia
  • In humans, ivabradine is an ‘open-channel’ blocker of hyperpolarization-activated cyclic nucleotide-gated channel isoform 4 (HCN4) (Bucchi 2006, 335) and I(f) current inhibitor
  • Ivabradine is an open channel blocker, which requires hyperpolarization; however, at the same time, block develops preferentially when channels deactivate at depolarized voltages. These apparently contradictory features provide ivabradine with a strong ‘use-dependence’ of f-channel block, since efficient block is favored by repetitive opening/closing cycles. Preferential block at depolarized voltages is a consequence of the fact that ivabradine molecules are positively charged and enter channel pores from their intracellular side. As a weak basic amine (pKa= 8.6), ivabradine is largely in the protonated form at the extracellular pH of 7.4 (94.1%); the fraction in the neutral form (5.9%) equilibrates across the membrane and enters the cell, where the largest fraction (96.2%) is again ionized at the intracellular pH of 7.2. However, experiments where the current flow through channels is varied independently of voltage (i.e. by means of channel block by Cs+ ions, or changes of external Na+ concentration) show that the block is not voltage dependent per se, but is rather ‘current’ dependent. These data can be explained by assuming that ivabradine molecules interact with permeating ions in one of their binding sites in the pore, and reveal that permeation across f-channels is likely to occur according to a multi-ion, single-file process[55]
  • Twelve healthy aging Beagle dogs, regardless of sex, were used with a mean age of 8.66±1.63 years. Basal anesthesia was induced followed by implantation of a pacemaker through the external jugular vein. All dogs underwent rapid right atrial pacing at a frequency of 600 beats/min for 2 months to induce the age-related AF model. The dogs were randomly divided into 2 groups – the Ivabradine group and the aging-AF group with 6 animals in each group. Ivabradine capsule (4 mg/kg/d) was orally administered to the dogs in the Ivabradine group during the pacing for 2 months, while no drug was provided to the aging-AF group (to see how both compared—treated patients vs. untreated patients with AF). As a result, ivabradine could effectively reduce the inducing rate of AF, and thus be used as an upstream drug for the prevention of age-related AF[56]

See also

[edit]

References

[edit]
  1. ^ Pratt, Donald Voet, Judith G. Voet, Charlotte W. (2013). Fundamentals of biochemistry : life at the molecular level (4th ed.). Hoboken, NJ: Wiley. p. 439. ISBN 978-0470-54784-7.{{cite book}}: CS1 maint: multiple names: authors list (link)
  2. ^ Rappay, Gyorgy; Nagy, Ivan; Makara, Gabor; Bacsy, Erno; Fazekas, Ilo Na (October 1979). "Major Metabolic Pathways and Hormone Production in Unstimulated Monolayer Cultures of the Rat Anterior Pituitary". In Vitro. 15 (10): 751–757. doi:10.1007/BF02618301. PMID 521036. S2CID 23206958.
  3. ^ Magasanik, Boris (June 8, 1953). "Metabolic Pathways of Glycerol Dissimilation: A Comparative Study of Two Strains of Aerobacter Aerogenes". Department of Bacteriology and Immunology, Harvard Medical School, Boston, Massachusetts. 66 (5): 611–619. doi:10.1128/jb.66.5.611-619.1953. PMC 317442. PMID 13108864.
  4. ^ Jagendorf, A. (September 1961). "The Quarterly Review of Biology". Chicago Journals.
  5. ^ O'Donnell, Michael M. Cox, Jennifer A. Doudna, Michael (2012). Molecular biology : principles and practice (1st printing. ed.). New York: W.H. Freeman and Co. ISBN 978-0-7167-7998-8.{{cite book}}: CS1 maint: multiple names: authors list (link)
  6. ^ al.], David Sadava ... [et (2014). Life : the science of biology (10th ed.). Sunderland, MA: Sinauer Associates. ISBN 978-1-4292-9864-3.
  7. ^ Klein, David (2012). Organic chemistry. Hoboken, N.J.: John Wiley. ISBN 978-0-471-75614-9.
  8. ^ Cheville, Norman F. (1994). Ultrastructural pathology: an introduction to interpretation (1st ed.). Ames: Iowa State University Press. ISBN 0813823986.
  9. ^ White, David (1995). The physiology and biochemistry of prokaryotes. New York [u.a.]: Oxford Univ. Press. ISBN 019508439X.
  10. ^ Kruger, ed. by Nicholas J.; Hill, Steve A.; Ratcliffe, R. George (1999). Regulation of primary metabolic pathways in plants : [proceedings of an international conference held on 9 - 11 January 1997 at St Hugh's College, Oxford under the auspices of the Phytochemical Society of Europe]. Dordrecht [u.a.]: Kluwer. ISBN 079235494X. {{cite book}}: |first1= has generic name (help)
  11. ^ a b "Metabolic pathway". Wikipedia, the free encyclopedia.
  12. ^ a b c Gould, ed. by Lawrence A. (1983). Drug treatment of cardiac arrhythmias. Mount Kisco: Futura Publishing Company. pp. 73–81. ISBN 0879931906. {{cite book}}: |first1= has generic name (help)
  13. ^ a b c Osadchii, Oleg E. (2014-08-01). "Procainamide and lidocaine produce dissimilar changes in ventricular repolarization and arrhythmogenicity in guinea-pig". Fundamental & Clinical Pharmacology. 28 (4): 382–393. doi:10.1111/fcp.12046. ISSN 1472-8206. PMID 23952942. S2CID 5086017.
  14. ^ Lee, Randall J. (March 1, 1992). "Relation Between Repolarization and Refractoriness in the Human Ventricle: Cycle Length Dependence and Effect of Procainamide". Journal of the American College of Cardiology. 19 (3): 614–618. doi:10.1016/S0735-1097(10)80281-5. PMID 1538018.
  15. ^ Zamponi, Gerald W. (1993). "Dual Actions of Procainamide on Batrachotoxin-activated Sodium Channels: Open Channel Block and Prevention of Inactivation". Biophysical Journal. 65 (6): 2333. doi:10.1016/S0006-3495(93)81291-8. PMC 1225974. PMID 8312472.
  16. ^ Szekely, Paul (October 17, 1953). "THE ACTION OF PROCAINE AND PROCAINE AMIDE ON THE HEART". Regional Cardiovascular Department, Newcastle General Hospital, and the Department OfPhysiology and Pharmacology, King's College, University of Durham: 267–272.
  17. ^ a b Gralinski, Michael R.; Chi, Liguo; Park, James L.; Friedrichs, Gregory S.; Tanhehco, Elaine J.; McCormack, James G.; Lucchesi, Benedict R. (2016-06-29). "Protective Effects of Ranolazine on Ventricular Fibrillation Induced by Activation of the ATP-Dependent Potassium Channel in the Rabbit Heart". Journal of Cardiovascular Pharmacology and Therapeutics. 1 (2): 141–148. doi:10.1177/107424849600100208. PMID 10684411. S2CID 33312985.
  18. ^ a b Carvas, Marcelo; Nascimento, Bruno C G; Acar, Mariana; Nearing, Bruce D; Belardinelli, Luiz; Verrier, Richard L (2010). "Intrapericardial Ranolazine Prolongs Atrial Refractory Period and Markedly Reduces Atrial Fibrillation Inducibility in the Intact Porcine Heart". Journal of Cardiovascular Pharmacology. 55 (3): 286–291. doi:10.1097/fjc.0b013e3181d26416. PMID 20075744. S2CID 32034249.
  19. ^ a b Banerjee, Kinjal; Ghosh, Raktim Kumar; Kamatam, Sravani; Banerjee, Arnab; Gupta, Anjan (2017). "Role of Ranolazine in cardiovascular disease and diabetes: Exploring beyond angina". International Journal of Cardiology. 227: 556–564. doi:10.1016/j.ijcard.2016.10.102. PMID 27838121.
  20. ^ Thomsen, Morten B. (2006). "Assessing the proarrhythmic potential of drugs: Current status of models and surrogate parameters of torsades de pointes arrhythmias". Pharmacology & Therapeutics. 112 (1): 151–163. doi:10.1016/j.pharmthera.2005.04.009. PMID 16714061.
  21. ^ Hwang, Hyun Seok; Hasdemir, Can; Laver, Derek; Mehra, Divya; Turhan, Kutsal; Faggioni, Michela; Yin, Huiyong; Knollmann, Björn C. (2011-04-01). "Inhibition of Cardiac Ca2+ Release Channels (RyR2) Determines Efficacy of Class I Antiarrhythmic Drugs in Catecholaminergic Polymorphic Ventricular TachycardiaClinical Perspective". Circulation: Arrhythmia and Electrophysiology. 4 (2): 128–135. doi:10.1161/CIRCEP.110.959916. ISSN 1941-3149. PMC 3667204. PMID 21270101.
  22. ^ "PROPAFENONE HYDROCHLORIDE TABLETS". www.accessdata.fda.gov. Retrieved 2017-03-27.
  23. ^ Campbell, J. K.; Marshall, R. J.; Winslow, E. (1991-10-01). "Comparison of the electrophysiological effects of Org 7797, disopyramide, mexiletine and propafenone in anaesthetized dogs with myocardial infarcts". British Journal of Pharmacology. 104 (2): 433–439. doi:10.1111/j.1476-5381.1991.tb12447.x. ISSN 0007-1188. PMC 1908530. PMID 1797309.
  24. ^ a b c d Suita, Kenji; Fujita, Takayuki; Hasegawa, Nozomi; Cai, Wenqian; Jin, Huiling; Hidaka, Yuko; Prajapati, Rajesh; Umemura, Masanari; Yokoyama, Utako (2015-07-23). "Norepinephrine-Induced Adrenergic Activation Strikingly Increased the Atrial Fibrillation Duration through β1- and α1-Adrenergic Receptor-Mediated Signaling in Mice". PLOS ONE. 10 (7): e0133664. doi:10.1371/journal.pone.0133664. ISSN 1932-6203. PMC 4512675. PMID 26203906.
  25. ^ Ablad, Bengt (1975). "Effects of metoprolol and propranolol on some metabolic responses to catecholamines in the anaesthetized dog". Department of Pharmacology and Medicine, AB Hassle, Fack, S-431 20 Molndal, Sweden. 36: 85–95.
  26. ^ Dosdall, Derek J.; Ranjan, Ravi; Higuchi, Koji; Kholmovski, Eugene; Angel, Nathan; Li, Li; MacLeod, Rob; Norlund, Layne; Olsen, Aaron (2013-09-01). "Chronic atrial fibrillation causes left ventricular dysfunction in dogs but not goats: experience with dogs, goats, and pigs". American Journal of Physiology - Heart and Circulatory Physiology. 305 (5): H725–H731. doi:10.1152/ajpheart.00440.2013. ISSN 0363-6135. PMC 4116536. PMID 23812387.
  27. ^ a b Waldo, Albert L. (1998). "Drug Treatment of Atrial Fibrillation in the Managed Care Era". Am J Cardiol. 81 (5A): 23C–29C. doi:10.1016/S0002-9149(98)00183-0. PMID 9525569.
  28. ^ Gould, ed. by Lawrence A. (1983). Drug treatment of cardiac arrhythmias. Mount Kisco: Futura Publishing Company. pp. 275–279. ISBN 0879931906. {{cite book}}: |first1= has generic name (help)
  29. ^ Van Herendael, Hugo; Dorian, Paul (2010-01-01). "Amiodarone for the treatment and prevention of ventricular fibrillation and ventricular tachycardia". Vascular Health and Risk Management. 6: 465–472. doi:10.2147/vhrm.s6611. ISSN 1176-6344. PMC 2922307. PMID 20730062.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  30. ^ a b c d e Harris, edited by Luke; Williams, Romeo Roncucci ; foreword by E.M. Vaughan (1986). Amiodarone : pharmacology, pharmacokinetics, toxicology, clinical effects. Paris: Médecine et sciences internationales. pp. 7–16. ISBN 2864391252. {{cite book}}: |first1= has generic name (help)CS1 maint: multiple names: authors list (link)
  31. ^ "FDA Product Insert for Amiodarone" (PDF). www.accessdata.fda.gov.
  32. ^ Li, Hongliang; Kim, Han Sol; Kim, Hye Won; Shin, Sung Eun; Jung, Won-Kyo; Ha, Kwon-Soo; Han, Eun-Taek; Hong, Seok-Ho; Firth, Amy L. (2016-07-01). "The class III anti-arrhythmic agent, amiodarone, inhibits voltage-dependent K+ channels in rabbit coronary arterial smooth muscle cells". Naunyn-Schmiedeberg's Archives of Pharmacology. 389 (7): 713–721. doi:10.1007/s00210-016-1232-8. ISSN 0028-1298. PMID 27030392. S2CID 6930665.
  33. ^ Hodeige, Dominique (February 24, 1995). "SR 33589, a new amiodarone-like antiarrhythmic agent: anti-adrenoceptor activity in anaesthetized and conscious dogs". European Journal of Pharmacology. 279 (1): 25–32. doi:10.1016/0014-2999(95)00130-D. PMID 7556379.
  34. ^ a b Doggrell, Sheila A.; Hancox, Jules C. (2004-04-01). "Dronedarone: an amiodarone analogue". Expert Opinion on Investigational Drugs. 13 (4): 415–426. doi:10.1517/13543784.13.4.415. ISSN 1354-3784. PMID 15102590. S2CID 13428408.
  35. ^ Castro, Antonio (February 2002). "New Antiarrhythmic Drugs for the Treatment of Atrial Fibrillation". Journal of Pacing and Clinical Electrophysiology. 25 (2): 249–259. doi:10.1046/j.1460-9592.2002.00249.x. PMID 11916001. S2CID 21636725.
  36. ^ "FDA Product Insert for Dronedarone" (PDF). www.accessdata.fda.gov.
  37. ^ Finance, Olivier (1995). "Effects of a new amiodarone-like agent, SR 33589, in comparison to amiodarone, D,L-sotalol, and lignocaine, on ischemia-induced ventricular arrhythmias in anesthetized pigs". Journal of Cardiovascular Pharmacology. 26 (4): 570–576. doi:10.1097/00005344-199510000-00010. PMID 8569217.
  38. ^ Manning, Allan (February 1995). "SR 33589, a new amiodarone-like antiarrhythmic agent: electrophysiological effects in anesthetized dogs". Journal of Cardiovascular Pharmacology. 25 (2): 252–261. doi:10.1097/00005344-199502000-00010. PMID 7752650. S2CID 25029457.
  39. ^ a b "FDA Product Insert for Sotalol" (PDF). www.accessdata.fda.gov.
  40. ^ Kpaeyeh, John Alvin; Wharton, John Marcus (2016). "Sotalol". Cardiac Electrophysiology Clinics. 8 (2): 437–452. doi:10.1016/j.ccep.2016.02.007. PMID 27261833.
  41. ^ Chiba, Toshiki; Kondo, Naoto; Takahara, Akira (2016-03-01). "Influences of rapid pacing-induced electrical remodeling on pharmacological manipulation of the atrial refractoriness in rabbits". Journal of Pharmacological Sciences. 130 (3): 170–176. doi:10.1016/j.jphs.2016.02.007. PMID 27032905.
  42. ^ Doggrell, Sheila A.; Hancox, Jules C. (2005-05-01). "Ibutilide – recent molecular insights and accumulating evidence for use in atrial flutter and fibrillation". Expert Opinion on Investigational Drugs. 14 (5): 655–669. doi:10.1517/13543784.14.5.655. ISSN 1354-3784. PMID 15926871. S2CID 34464213.
  43. ^ "Product Monograph: Covert (Ibutilide Fumarate)" (PDF).
  44. ^ Cimini, Madeline G.; Brunden, Marshall N.; Gibson, J.Kenneth (1992). "Effects of ibutilide fumarate, a novel antiarrhythmic agent, and its enantiomers on isolated rabbit myocardium". European Journal of Pharmacology. 222 (1): 93–98. doi:10.1016/0014-2999(92)90467-i. PMID 1361444.
  45. ^ Buchanan, Lewis V.; Le May, Richelle J.; Walters, Rodney R.; Hsu, Chang-Yuan L.; Brunden, Marshal N.; Gibson, John K. (1996-02-01). "Antiarrhythmic and Electrophysiologic Effects of Intravenous Ibutilide and Sotaloi in the Canine Sterile Pericarditis Model". Journal of Cardiovascular Electrophysiology. 7 (2): 113–119. doi:10.1111/j.1540-8167.1996.tb00506.x. ISSN 1540-8167. PMID 8853021. S2CID 21962707.
  46. ^ Morel, Nicole; Buryi, Vitali; Feron, Olivier; Gomez, Jean-Pierre; Christen, Marie-Odile; Godfraind, Théophile (1998-11-01). "The action of calcium channel blockers on recombinant L-type calcium channel α1-subunits". British Journal of Pharmacology. 125 (5): 1005–1012. doi:10.1038/sj.bjp.0702162. ISSN 1476-5381. PMC 1565671. PMID 9846638.
  47. ^ "Covera Product Insert" (PDF).
  48. ^ Curtis, M. J.; Walker, M. J. (1986-09-01). "The mechanism of action of the optical enantiomers of verapamil against ischaemia-induced arrhythmias in the conscious rat". British Journal of Pharmacology. 89 (1): 137–147. doi:10.1111/j.1476-5381.1986.tb11129.x. ISSN 0007-1188. PMC 1917029. PMID 3801768.
  49. ^ Andronache, Zoita; Ursu, Daniel; Lehnert, Simone; Freichel, Marc; Flockerzi, Veit; Melzer, Werner (2007-11-06). "The auxiliary subunit γ1 of the skeletal muscle L-type Ca2+ channel is an endogenous Ca2+ antagonist". Proceedings of the National Academy of Sciences. 104 (45): 17885–17890. doi:10.1073/pnas.0704340104. ISSN 0027-8424. PMC 2077065. PMID 17978188.
  50. ^ "Cardizem Product Insert" (PDF).
  51. ^ Noda, Yoshiaki; Hashimoto, Keitaro (2004-01-01). "Development of a Halothane-Adrenaline Arrhythmia Model Using In Vivo Guinea Pigs". Journal of Pharmacological Sciences. 95 (2): 234–239. doi:10.1254/jphs.FP0030423. PMID 15215648. S2CID 23090634.
  52. ^ Schwarzwald, Colin C.; Bonagura, John D.; Luis-Fuentes, Virginia (2005-09-01). "Effects of diltiazem on hemodynamic variables and ventricular function in healthy horses". Journal of Veterinary Internal Medicine. 19 (5): 703–711. doi:10.1892/0891-6640(2005)19[703:eodohv]2.0.co;2. ISSN 0891-6640. PMID 16231715.
  53. ^ Archer, S L; Huang, J M; Hampl, V; Nelson, D P; Shultz, P J; Weir, E K (1994-08-02). "Nitric oxide and cGMP cause vasorelaxation by activation of a charybdotoxin-sensitive K channel by cGMP-dependent protein kinase". Proceedings of the National Academy of Sciences of the United States of America. 91 (16): 7583–7587. doi:10.1073/pnas.91.16.7583. ISSN 0027-8424. PMC 44446. PMID 7519783.
  54. ^ Fenelon, Guilherme; Protter, Andrew A.; Stambler, Bruce S. (2002). "Examination of the in vivo cardiac electrophysiological effects of nesiritide (human brain natriuretic peptide) in conscious dogs". Journal of Cardiac Failure. 8 (5): 320–325. doi:10.1054/jcaf.2002.127772. PMID 12411983.
  55. ^ Bucchi, A.; Tognati, A.; Milanesi, R.; Baruscotti, M.; DiFrancesco, D. (2006-04-01). "Properties of ivabradine-induced block of HCN1 and HCN4 pacemaker channels". The Journal of Physiology. 572 (2): 335–346. doi:10.1113/jphysiol.2005.100776. ISSN 1469-7793. PMC 1779671. PMID 16484306.
  56. ^ Tang, Bao-Peng (2015-05-16). "Effects of Ivabradine on Cardiac Electrophysiology in Dogs with Age-Related Atrial Fibrillation". Medical Science Monitor. 21: 1414–1420. doi:10.12659/msm.894320. ISSN 1234-1010. PMC 4444168. PMID 25982136.

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