Acidosis inhibits spontaneous activity and membrane currents in myocytes isolated from the rabbit atrioventricular node.
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[1] H. Cingolani,et al. Acidosis and arrhythmias in cardiac muscle. , 1994, Cardiovascular research.
[2] E. Carmeliet,et al. The effect of external pH on the delayed rectifying K+ current in cardiac ventricular myocytes , 2000, Pflügers Archiv.
[3] S M Cobbe,et al. Adenosine increases potassium conductance in isolated rabbit atrioventricular nodal myocytes. , 1995, Cardiovascular research.
[4] Yi-Mei Du,et al. Ionic basis of ischemia-induced bradycardia in the rabbit sinoatrial node. , 2007, Journal of molecular and cellular cardiology.
[5] D. Noble,et al. Displacement of activator thresholds in cardiac muscle by protons and calcium ions. , 1978, The Journal of physiology.
[6] In vitro and in vivo electrocardiographic evaluation of the novel calcium antagonist monatepil on cardiac conduction system. , 1993, Arzneimittel-Forschung.
[7] O Gryshchenko,et al. Ischemia alters the electrical activity of pacemaker cells isolated from the rabbit sinoatrial node. , 2002, American journal of physiology. Heart and circulatory physiology.
[8] A. Workman,et al. Rate-dependency of action potential duration and refractoriness in isolated myocytes from the rabbit AV node and atrium. , 2000, Journal of molecular and cellular cardiology.
[9] Robert H. Anderson,et al. A Combined Morphological and Electrophysiological Study of the Atrioventricular Node of the Rabbit Heart , 1974, Circulation research.
[10] G. Rozanski,et al. Acidosis masks beta-adrenergic control of cardiac L-type calcium current. , 1995, Journal of molecular and cellular cardiology.
[11] Yi-Mei Du,et al. Simulated ischemia enhances L-type calcium current in pacemaker cells isolated from the rabbit sinoatrial node. , 2007, American journal of physiology. Heart and circulatory physiology.
[12] J. T. Hulme,et al. Effect of acidosis on transient outward potassium current in isolated rat ventricular myocytes. , 2000, American Journal of Physiology. Heart and Circulatory Physiology.
[13] H. Hayakawa,et al. Use of intravenous dofetilide in atrial flutter with hemodynamic instability. , 1996, Japanese circulation journal.
[14] H. Irisawa,et al. Transient Outward Current Carried by Potassium and Sodium in Quiescent Atrioventricular Node Cells of Rabbits , 1985, Circulation research.
[15] C. Orchard,et al. The Effect of Acidosis on the Ecg of the Rat Heart , 2001, Experimental physiology.
[16] J. Jalife,et al. Proton and zinc effects on HERG currents. , 1999, Biophysical journal.
[17] M. Boyett,et al. Characterization of the effects of ryanodine, TTX, E-4031 and 4-AP on the sinoatrial and atrioventricular nodes. , 2008, Progress in biophysics and molecular biology.
[18] J. Hancox,et al. Inhibition of L‐type calcium current by propafenone in single myocytes isolated from the rabbit atrioventricular node , 1997, British journal of pharmacology.
[19] I. Efimov,et al. Optical mapping of the atrioventricular junction. , 2005, Journal of electrocardiology.
[20] J. Kentish,et al. Effects of changes of pH on the contractile function of cardiac muscle. , 1990, The American journal of physiology.
[21] M. Boyett,et al. Contraction and intracellular Ca2+, Na+, and H+ during acidosis in rat ventricular myocytes. , 1992, The American journal of physiology.
[22] C. Orchard,et al. Compensatory role of CaMKII on ICa and SR function during acidosis in rat ventricular myocytes , 2001, Pflügers Archiv.
[23] R. Beňačka,et al. [Disorders of heart rhythm and ECG changes in experimental apneic states]. , 1997, Bratislavske lekarske listy.
[24] Robert H. Anderson. Das reizleitungssystem des säugetierherzens: S. Tawara Gustav Fischer, Jena, 1906; 193 pp.; , 1988 .
[25] A Shrier,et al. Sodium Channel Distribution Within the Rabbit Atrioventricular Node as Analysed by Confocal Microscopy , 1997, The Journal of physiology.
[26] J. Hancox,et al. The actions of nickel on membrane currents activated by hyperpolarisation in single cells from the rabbit atrioventricular node. , 1995, General pharmacology.
[27] Montoya,et al. Aspirin Intoxication in a Child Associated with Myocardial Necrosis: Is This a Drug-related Lesion? , 2003, Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society.
[28] G. Rozanski,et al. Acidosis masks β-adrenergic control of cardiac L-type calcium current , 1995 .
[29] Godfrey L. Smith,et al. Acidosis delays conduction through the atrioventricular node , 2007 .
[30] E. Cingolani,et al. Chronotropic response of isolated atria to acid base alterations. , 1978, Archives internationales de physiologie et de biochimie.
[31] M J Janse,et al. Morphology and electrophysiology of the mammalian atrioventricular node. , 1988, Physiological reviews.
[32] M. Sanguinetti,et al. Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents , 1990, The Journal of general physiology.
[33] W. L. Nelson,et al. The Pharmacokinetics and Pharmacodynamics of d- and dl-Verapamil in Rabbits , 1985, Journal of cardiovascular pharmacology.
[34] W. Ho,et al. Blockade of HERG channels expressed in Xenopus oocytes by external H+ , 1999, Pflügers Archiv.
[35] C. Orchard,et al. Electrophysiological response of rat ventricular myocytes to acidosis. , 2002, American journal of physiology. Heart and circulatory physiology.
[36] J. Hancox,et al. An investigation of the role played by the E-4031-sensitive (rapid delayed rectifier) potassium current in isolated rabbit atrioventricular nodal and ventricular myocytes , 1999, Pflügers Archiv.
[37] Bernd Lindemann,et al. Hyperpolarization-activated channels HCN1 and HCN4 mediate responses to sour stimuli , 2001, Nature.
[38] S. Houser,et al. Acidosis facilitates spontaneous sarcoplasmic reticulum Ca2+ release in rat myocardium , 1987, The Journal of general physiology.
[39] R. Lazzara,et al. Effect of GLG-V-13, a class III antiarrhythmic agent, on potassium currents in rabbit ventricular myocytes. , 2000, Life sciences.
[40] A J Levi,et al. L-type calcium current in rod- and spindle-shaped myocytes isolated from rabbit atrioventricular node. , 1994, The American journal of physiology.
[41] P. Daleau,et al. Modulation of HERG potassium channel properties by external pH , 1999, Pflügers Archiv.
[42] J. Hancox,et al. A method for making rapid changes of superfusate whilst maintaining temperature at 37°C , 1996, Pflügers Archiv.
[43] Jules C. Hancox,et al. Progress and Gaps in Understanding the Electrophysiological Properties of Morphologically Normal Cells from the Cardiac atrioventricular Node , 2003, Int. J. Bifurc. Chaos.
[44] W. Giles,et al. Electrophysiological effects of ibutilide on the delayed rectifier K(+) current in rabbit sinoatrial and atrioventricular node cells. , 2000, European journal of pharmacology.
[45] A Shrier,et al. Electrophysiological properties of morphologically distinct cells isolated from the rabbit atrioventricular node. , 1996, The Journal of physiology.
[46] D. Zipes,et al. Action of Manganese Ions and Tetrodotoxin on Atrioventricular Nodal Transmembrane Potentials in Isolated Rabbit Hearts , 1973, Circulation research.
[47] Jules C. Hancox,et al. A method for isolating rabbit atrioventricular node myocytes which retain normal morphology and function. , 1993, The American journal of physiology.
[48] Shi-sheng Zhou,et al. Morphological and electrophysiological properties of single myocardial cells from Koch triangle of rabbit heart , 2006, Chinese medical journal.
[49] H. Satoh,et al. On the mechanism by which changes in extracellular pH affect the electrical activity of the rabbit sino‐atrial node. , 1986, The Journal of physiology.
[50] G. Isenberg,et al. Calcium tolerant ventricular myocytes prepared by preincubation in a “KB medium” , 1982, Pflügers Archiv.
[51] R. Vaughan-Jones,et al. Application of a new pH-sensitive fluoroprobe (carboxy-SNARF-1) for intracellular pH measurement in small, isolated cells , 1990, Pflügers Archiv.
[52] K. Hashimoto,et al. Effect of pH on the sino-atrial node cells and atrial muscle of dog. , 1983, Archives internationales de pharmacodynamie et de therapie.
[53] A. Workman,et al. Ionic basis of a differential effect of adenosine on refractoriness in rabbit AV nodal and atrial isolated myocytes. , 1999, Cardiovascular research.
[54] E. Grenadier,et al. Complete atrioventricular block, shock, and hyperkalemia induced by toxic adenoma of the thyroid gland. , 1981, Heart & lung : the journal of critical care.
[55] Jules C. Hancox,et al. Characteristics of the delayed rectifier K current compared in myocytes isolated from the atrioventricular node and ventricle of the rabbit heart , 1996, Pflügers Archiv.
[56] J. Hancox,et al. The hyperpolarisation-activated current,If, is not required for pacemaking in single cells from the rabbit atrioventricular node , 1994, Pflügers Archiv.
[57] J. Hancox,et al. A method for making rapid changes of superfusate whilst maintaining temperature at 37 degrees C. , 1996, Pflugers Archiv : European journal of physiology.
[58] A J Levi,et al. Actions of the digitalis analogue strophanthidin on action potentials and L‐type calcium current in single cells isolated from the rabbit atrioventricular node , 1996, British journal of pharmacology.
[59] R. Anderson,et al. Histologic and histochemical evidence concerning the presence of morphologically distinct cellular zones within the rabbit atrioventricular node , 1972, The Anatomical record.
[60] John S. Mitcheson,et al. Characteristics of a transient outward current (sensitive to 4-aminopyridine) in Ca2+-tolerant myocytes isolated from the rabbit atrioventricular node , 1999, Pflügers Archiv.
[61] Yoshihisa Kurachi,et al. Action potential and membrane currents of single pacemaker cells of the rabbit heart , 1984, Pflügers Archiv.
[62] R. Lazzara,et al. Electrophysiological and inotropic characterization of a novel class III antiarrhythmic agent, GLG-V-13, in the mammalian heart. , 1996, Journal of cardiovascular pharmacology.
[63] W R Giles,et al. [Electrophysiological heterogeneity of rabbit atrioventricular node cells: possible relationship to fast and slow pathways]. , 1998, Journal of cardiology.
[64] D P Zipes,et al. Effects of Agents which Inhibit the Slow Channel on Sinus Node Automaticity and Atrioventricular Conduction in the Dog , 1974, Circulation research.
[65] J. Hancox,et al. Na‐Ca Exchange Tail Current Indicates Voltage Dependence of the Cai Transient in Rabbit Ventricular Myocytes , 1995, Journal of cardiovascular electrophysiology.