PHARMACOLOGICAL ANALYSIS OF ESTABLISHED VENTRICULAR-FIBRILLATION

EJF CARLISLE, JD ALLEN, George Kernohan, W LEAHEY, AAJ ADGEY

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium.
LanguageEnglish
Pages530-534
JournalBritish Journal of Pharmacology
Volume100
Issue number3
Publication statusPublished - Jul 1990

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Ventricular Fibrillation
Endocardium
Pharmacology
Pharmaceutical Preparations
Sodium Channels
Anti-Arrhythmia Agents
Pentobarbital
Calcium Channels
Verapamil
Lidocaine
Propranolol
Electric Stimulation
Lead
Sodium
Dogs
Calcium

Cite this

CARLISLE, EJF., ALLEN, JD., Kernohan, G., LEAHEY, W., & ADGEY, AAJ. (1990). PHARMACOLOGICAL ANALYSIS OF ESTABLISHED VENTRICULAR-FIBRILLATION. British Journal of Pharmacology, 100(3), 530-534.
CARLISLE, EJF ; ALLEN, JD ; Kernohan, George ; LEAHEY, W ; ADGEY, AAJ. / PHARMACOLOGICAL ANALYSIS OF ESTABLISHED VENTRICULAR-FIBRILLATION. In: British Journal of Pharmacology. 1990 ; Vol. 100, No. 3. pp. 530-534.
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abstract = "1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium.",
author = "EJF CARLISLE and JD ALLEN and George Kernohan and W LEAHEY and AAJ ADGEY",
note = "Reference text: ADGEY, A.A.J., ALLEN, J.D., CARLISLE, E.J.F., KERNOHAN, W.G. & LEAHEY, W. (1987). Effects of anti-arrhythmic drugs on established ventricular fibrillation in the anaesthetized dog. J. Physiol., 392, 79P. ANDERSON, J.L., PATTERSON, E., CONLON, M., PASYK, S., PInT, B. & LUCCHESI, B.R. (1980). Kinetics of antifibrillatory effects of bretylium: correlation with myocardial drug concentrations. Am. J. Cardiol., 46, 583-592. BIGGER, J.T., JR. & JAFFE, C.C. (1971). The effect of bretylium tosylate on electrophysiological properties of ventricular muscle and Purkinje fibres. Am. J. Cardiol., 27, 82-92. CARLISLE, E.J.F., ALLEN, J.D., KERNOHAN, W.G., ANDERSON, J. & ADGEY, A.A.J. (1990). Fourier analysis of ventricular fibrillation of varied aetiology. Eur. Heart J., 11, 173-181. CHEUNG, J.Y., BONVENTRE, J.V., MALIS, C.D. & LEAF, A. (1986). Calcium and ischemic injury. N. Engl. J. Med., 314, 1670-1676. CLARK, R.E., FERGUSON, T.B., WEST, P.N., SCHUCHLIEB, R.C. & HENRY, P.D. (1977). Pharmacological preservation of the ischemic heart. Ann. Thorac. Surg., 24, 307-314. COLTART, D.J. & SHAND, D.G. (1970). Plasma propranolol levels in the quantitative assessment of beta adrenergic blockade in man. Br. Med. J., 3, 731-734. DAHL, G. & ISENBERG, G. (1980). Decoupling of heart muscle cells: correlation with increased cytoplasmic calcium activity and with changes of nexus ultrastructure. J. Memb. Biol., 53, 63-75. DAVIS, L.D. & TEMTE, J.V. (1968). Effects of propranolol on the transmembrane potentials of ventricular muscle and Purkinje fibers of the dog. Circ. Res., 22, 661-677. DE MELLO, W.C. (1976). Influence of the sodium pump on intercellular communication in heart fibres: effect of intracellular injection of sodium ion on electrical coupling. J. Phyisol., 263, 171-197. ELHARRAR, V., GAUM, W.E. & ZIPES, D.P. (1977). Effect of drugs on conduction delay and incidence of ventricular arrhythmias induced by acute coronary occlusion in dogs. Am. J. Cardiol., 39, 544-549. FIRST INTERNATIONAL STUDY OF INFARCT SURVIVAL COLLABORATIVE GROUP (1986). Randomised trial of intravenous atenolol among 16027 cases of suspected acute myocardial infarction: ISIS 1. Lancet, ii, 57-65. FLEET, W.F., JOHNSON, T.A., GRAEBNER, C.A., ENGLE, C.L. & GETTES, L.S. (1986). Effects of verapamil on ischemia-induced changes in extracellular K+, pH and local activation in the pig. Circulation, 73, 837-846. GEUZE, R.H. & DEVENTE, J. (1983). Effects of duration of ventricular fibrillation and heart massage on haemodynamic responses after defibrillation in dogs. Cardiovasc. Res., 17, 282-289. GILMORE, J.P. & SIEGEL, J.H. (1962). Mechanism of the myocardial effects of bretylium. Circ. Res., 10, 347-353. HIRATA, Y., KODAMA, I., IWAMURA, N., SHIMIZU, T., TOYAMA, J. & YAMADA, K. (1979). Effects of verapamil on canine Purkinje fibres 534 E.J.F. CARLISLE et al. and ventricular muscle fibres with particular reference to the alternation of action potential duration after a sudden increase in driving rate. Cardiovasc. Res., 13, 1-8. KUPERSMITH, J. (1979). Electrophysiological and antiarrhythmic effects of lidocaine in canine acute myocardial ischemia. Am. Heart J., 97, 360-366. LITTLE, R.A., FRAYN, K.N., RANDALL, P.E., STONER, H.B., YATES, D.W., LAING, G.S., KUMAR, S. & BANKS, J.M. (1985). Plasma catecholamines in patients with acute myocardial infarction and cardiac arrest. Quart. J. Med., 54, 133-140. MARTIN, G., COSIN, J., SUCH, M., HERNANDEZ, A. & LLAMAS, P. (1986). Relation between power spectrum time course during ventricular fibrillation and electromechanical dissociation. Effects of coronary perfusion and nifedipine. Eur. Heart J., 7, 560-569. PANTRIDGE, J.F., WEBB, S.W., ADGEY, A.A.J. & GEDDES, J.S. (1974). The first hour after the onset of acute myocardial infarction. In Progress in Cardiology, vol 3. ed. Yu, P.N. & Goodwin, J.F. pp. 173-188. Philadelphia: Lea and Febiger. REIMER, K.A., LOWE, J.E. & JENNINGS, R.B. (1977). Effect of the calcium antagonist verapamil on necrosis following temporary coronary artery occlusion in dogs. Circulation, 55, 581-587. REIMER, K.A., RASMUSSEN, M.M. & JENNINGS, R.B. (1973). Reduction by propranolol of myocardial necrosis following temporary coronary artery occlusion in dogs. Circ. Res., 33, 353-363. ROSEN, M.R., HOFFMAN, B.F. & WIT, A.L. (1975). Electrophysiology and pharmacology of cardiac arrhythmias. V. Cardiac antiarrhythmic effects of lidocaine. Am. Heart J., 89, 526-536. SANNA; G. & ARCIDIACONO, R. (1973). Chemical ventricular defibrillation of the human heart with bretylium tosylate. Am. J. Cardiol., 32, 982-987. SINGH, B.N. & NADAMANEE, K. (1982). The electrophysiological classification of antiarrhythmic drugs. In Recent Developments in Cardiovascular Drugs. ed. Coltart, J. & Jewitt, D. pp. 73-77. Edinburgh: Churchill-Livingstone. SINGH, B.N. & VAUGHAN-WILLAIMS, E.M. (1971). Effect of altering potassium concentration on the action of lidocaine and diphenylhydantoin on rabbit atrial and ventricular muscle. Circ. Res., 29, 286-295. SINGH, B.N. & VAUGHAN WILLIAMS, E.M. (1972). A fourth class of antidysrhythmic action. Effect of verapamil on ouabain toxicity, on atrial and ventricular intracellular potentials, and on other features of cardiac function. Cardiovasc. Res., 6, 109-119. TAGGART, P., DONALDSON, R., ABED, J. & NASHAT, F. (1984). Class III action of beta-blocking agents. Cardiovasc. Res., 18, 683-689. VAUGHAN WILLIAMS, E.M. (1984). A classification of antiarrhythmic actions reassessed after a decade of new drugs. J. Clin. Pharmacol., 24, 129-147. WORLEY, S.J., SWAIN, J.L., COLAVITA, P.G., SMITH, W.M. & IDEKER, R.E. (1985). Development of an endocardial-epicardial gradient of activation rate during electrically-induced, sustained ventricular fibrillation. Am. J. Cardiol., 55, 813-820.",
year = "1990",
month = "7",
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volume = "100",
pages = "530--534",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
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}

CARLISLE, EJF, ALLEN, JD, Kernohan, G, LEAHEY, W & ADGEY, AAJ 1990, 'PHARMACOLOGICAL ANALYSIS OF ESTABLISHED VENTRICULAR-FIBRILLATION', British Journal of Pharmacology, vol. 100, no. 3, pp. 530-534.

PHARMACOLOGICAL ANALYSIS OF ESTABLISHED VENTRICULAR-FIBRILLATION. / CARLISLE, EJF; ALLEN, JD; Kernohan, George; LEAHEY, W; ADGEY, AAJ.

In: British Journal of Pharmacology, Vol. 100, No. 3, 07.1990, p. 530-534.

Research output: Contribution to journalArticle

TY - JOUR

T1 - PHARMACOLOGICAL ANALYSIS OF ESTABLISHED VENTRICULAR-FIBRILLATION

AU - CARLISLE, EJF

AU - ALLEN, JD

AU - Kernohan, George

AU - LEAHEY, W

AU - ADGEY, AAJ

N1 - Reference text: ADGEY, A.A.J., ALLEN, J.D., CARLISLE, E.J.F., KERNOHAN, W.G. & LEAHEY, W. (1987). Effects of anti-arrhythmic drugs on established ventricular fibrillation in the anaesthetized dog. J. Physiol., 392, 79P. ANDERSON, J.L., PATTERSON, E., CONLON, M., PASYK, S., PInT, B. & LUCCHESI, B.R. (1980). Kinetics of antifibrillatory effects of bretylium: correlation with myocardial drug concentrations. Am. J. Cardiol., 46, 583-592. BIGGER, J.T., JR. & JAFFE, C.C. (1971). The effect of bretylium tosylate on electrophysiological properties of ventricular muscle and Purkinje fibres. Am. J. Cardiol., 27, 82-92. CARLISLE, E.J.F., ALLEN, J.D., KERNOHAN, W.G., ANDERSON, J. & ADGEY, A.A.J. (1990). Fourier analysis of ventricular fibrillation of varied aetiology. Eur. Heart J., 11, 173-181. CHEUNG, J.Y., BONVENTRE, J.V., MALIS, C.D. & LEAF, A. (1986). Calcium and ischemic injury. N. Engl. J. Med., 314, 1670-1676. CLARK, R.E., FERGUSON, T.B., WEST, P.N., SCHUCHLIEB, R.C. & HENRY, P.D. (1977). Pharmacological preservation of the ischemic heart. Ann. Thorac. Surg., 24, 307-314. COLTART, D.J. & SHAND, D.G. (1970). Plasma propranolol levels in the quantitative assessment of beta adrenergic blockade in man. Br. Med. J., 3, 731-734. DAHL, G. & ISENBERG, G. (1980). Decoupling of heart muscle cells: correlation with increased cytoplasmic calcium activity and with changes of nexus ultrastructure. J. Memb. Biol., 53, 63-75. DAVIS, L.D. & TEMTE, J.V. (1968). Effects of propranolol on the transmembrane potentials of ventricular muscle and Purkinje fibers of the dog. Circ. Res., 22, 661-677. DE MELLO, W.C. (1976). Influence of the sodium pump on intercellular communication in heart fibres: effect of intracellular injection of sodium ion on electrical coupling. J. Phyisol., 263, 171-197. ELHARRAR, V., GAUM, W.E. & ZIPES, D.P. (1977). Effect of drugs on conduction delay and incidence of ventricular arrhythmias induced by acute coronary occlusion in dogs. Am. J. Cardiol., 39, 544-549. FIRST INTERNATIONAL STUDY OF INFARCT SURVIVAL COLLABORATIVE GROUP (1986). Randomised trial of intravenous atenolol among 16027 cases of suspected acute myocardial infarction: ISIS 1. Lancet, ii, 57-65. FLEET, W.F., JOHNSON, T.A., GRAEBNER, C.A., ENGLE, C.L. & GETTES, L.S. (1986). Effects of verapamil on ischemia-induced changes in extracellular K+, pH and local activation in the pig. Circulation, 73, 837-846. GEUZE, R.H. & DEVENTE, J. (1983). Effects of duration of ventricular fibrillation and heart massage on haemodynamic responses after defibrillation in dogs. Cardiovasc. Res., 17, 282-289. GILMORE, J.P. & SIEGEL, J.H. (1962). Mechanism of the myocardial effects of bretylium. Circ. Res., 10, 347-353. HIRATA, Y., KODAMA, I., IWAMURA, N., SHIMIZU, T., TOYAMA, J. & YAMADA, K. (1979). Effects of verapamil on canine Purkinje fibres 534 E.J.F. CARLISLE et al. and ventricular muscle fibres with particular reference to the alternation of action potential duration after a sudden increase in driving rate. Cardiovasc. Res., 13, 1-8. KUPERSMITH, J. (1979). Electrophysiological and antiarrhythmic effects of lidocaine in canine acute myocardial ischemia. Am. Heart J., 97, 360-366. LITTLE, R.A., FRAYN, K.N., RANDALL, P.E., STONER, H.B., YATES, D.W., LAING, G.S., KUMAR, S. & BANKS, J.M. (1985). Plasma catecholamines in patients with acute myocardial infarction and cardiac arrest. Quart. J. Med., 54, 133-140. MARTIN, G., COSIN, J., SUCH, M., HERNANDEZ, A. & LLAMAS, P. (1986). Relation between power spectrum time course during ventricular fibrillation and electromechanical dissociation. Effects of coronary perfusion and nifedipine. Eur. Heart J., 7, 560-569. PANTRIDGE, J.F., WEBB, S.W., ADGEY, A.A.J. & GEDDES, J.S. (1974). The first hour after the onset of acute myocardial infarction. In Progress in Cardiology, vol 3. ed. Yu, P.N. & Goodwin, J.F. pp. 173-188. Philadelphia: Lea and Febiger. REIMER, K.A., LOWE, J.E. & JENNINGS, R.B. (1977). Effect of the calcium antagonist verapamil on necrosis following temporary coronary artery occlusion in dogs. Circulation, 55, 581-587. REIMER, K.A., RASMUSSEN, M.M. & JENNINGS, R.B. (1973). Reduction by propranolol of myocardial necrosis following temporary coronary artery occlusion in dogs. Circ. Res., 33, 353-363. ROSEN, M.R., HOFFMAN, B.F. & WIT, A.L. (1975). Electrophysiology and pharmacology of cardiac arrhythmias. V. Cardiac antiarrhythmic effects of lidocaine. Am. Heart J., 89, 526-536. SANNA; G. & ARCIDIACONO, R. (1973). Chemical ventricular defibrillation of the human heart with bretylium tosylate. Am. J. Cardiol., 32, 982-987. SINGH, B.N. & NADAMANEE, K. (1982). The electrophysiological classification of antiarrhythmic drugs. In Recent Developments in Cardiovascular Drugs. ed. Coltart, J. & Jewitt, D. pp. 73-77. Edinburgh: Churchill-Livingstone. SINGH, B.N. & VAUGHAN-WILLAIMS, E.M. (1971). Effect of altering potassium concentration on the action of lidocaine and diphenylhydantoin on rabbit atrial and ventricular muscle. Circ. Res., 29, 286-295. SINGH, B.N. & VAUGHAN WILLIAMS, E.M. (1972). A fourth class of antidysrhythmic action. Effect of verapamil on ouabain toxicity, on atrial and ventricular intracellular potentials, and on other features of cardiac function. Cardiovasc. Res., 6, 109-119. TAGGART, P., DONALDSON, R., ABED, J. & NASHAT, F. (1984). Class III action of beta-blocking agents. Cardiovasc. Res., 18, 683-689. VAUGHAN WILLIAMS, E.M. (1984). A classification of antiarrhythmic actions reassessed after a decade of new drugs. J. Clin. Pharmacol., 24, 129-147. WORLEY, S.J., SWAIN, J.L., COLAVITA, P.G., SMITH, W.M. & IDEKER, R.E. (1985). Development of an endocardial-epicardial gradient of activation rate during electrically-induced, sustained ventricular fibrillation. Am. J. Cardiol., 55, 813-820.

PY - 1990/7

Y1 - 1990/7

N2 - 1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium.

AB - 1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium.

M3 - Article

VL - 100

SP - 530

EP - 534

JO - British Journal of Pharmacology

T2 - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

IS - 3

ER -

CARLISLE EJF, ALLEN JD, Kernohan G, LEAHEY W, ADGEY AAJ. PHARMACOLOGICAL ANALYSIS OF ESTABLISHED VENTRICULAR-FIBRILLATION. British Journal of Pharmacology. 1990 Jul;100(3):530-534.