Role of some components of ischemia in the genesis of spontaneous ventricular arrhythmias

Archiv für Kreislaufforschung - Tập 79 - Trang 68-74 - 1984
J. Senges1,2, H. Seller1,2, J. Brachmann1,2, W. Braun1,2, E. Mayer1,2, I. Rizos1,2, W. Kübler1,2
1Abteilung Innere Medizin III (Kardiologie) of the Medizinische Klinik, Universität Heidelberg, Heidelberg, FRG
2II. Physiologisches Institut, Universität Heidelberg, Heidelberg FRG

Tóm tắt

The importance of single components of ischemia including hypoxia, lactic acidosis, high potassium, and sympathetic stimulation to the spontaneous occurrence of ventricular arrhythmias was studied in chloralose-anesthetized cats using systemic and local intracoronary administration. Hypoxia and acidosis provoked no spontaneous arrhythmias regardless of systemic or regional administration. Systemic or local hyperpotassemia induced regularly ventricular ectopic activity including recurrent ventricular tachycardias that were characterized by a sudden onset and termination and by a stable rate. Stimulation of the left, right or bilateral stellate ganglia failed to provoke ventricular arrhythmias during hypoxia or acidosis and had also no influence on the initiation or rate of K+-induced ventricular tachycardias. The results indicate that high extracellular K+ may be the predominant arrhythmogenic factor of the components of ischemia we studied and that sympathetic ganglia stimulation does not affect K+-induced ventricular tachycardia.

Tài liệu tham khảo

Antoni H, Zerweck T (1967) Besitzen die sympathischen Überträgerstoffe einen direkten Einfluß auf die Leitungsgeschwindigkeit des Säugetiermyokards? Pflügers Arch 293:310–330 Brachmann J, Scherlag J, Harrison LA, Berbari EJ, Lazzara R (1981) Epinephrine selectively improves electrical function in the infarcted dog heart. Circulation 69, Suppl IV, IV-320 Brown RH, Noble D (1972) Effect of pH on ionic currents underlying pacemaker activity in cardiac Purkinje fibers. J Physiol 224:39P-40P Cranefield PF, Hoffman BF (1971) Conduction of the cardiac impulse: II. Summation and inhibition. Circ Res 28:220–233 Cranefield PF, Klein HO, Hoffman BF (1971) Conduction of the cardiac impulse: I. Delay, block and one-way block in depressed Purkinje fibers. Circ Res 28:199–219 Cranefield PF, Wit AL, Hoffman BF (1972) Conduction of cardiac impulses: III. Characteristics of very slow conduction. J Gen Physiol 59:227–246 Cranefield PF (1975) The conduction of the cardiac impulse. Future Publishing C, New York Downar E, Janse MJ, Durrer D (1977) The effect of “ischemic” blood on transmembrane potentials of normal porcine ventricular myocardium. Circulation 55:455–462 Engstfeld G, Antoni H, Fleckenstein A, Nast A, Hattingberg M v (1961) Die Restitution der Erregungsfortleitung und Kontraktionskraft des K+-gelähmten Frosch- und Säugetiermyokards durch Adrenalin. Pflügers Arch 273:145–163 Fozzard HA (1975) Validity of myocardial infarction models. Circulation 51/52 Suppl III, 131–138 Hirche HJ, Franz Chr, Bös L, Bissig R, Lang R, Schramm M (1980) Myocardial extracellular K+ and H+ increase and noradrenaline release as possible cause of early arrhythmias following acute coronary artery occlusion in pigs. J Mol Cell Cardiol 12:579–593 Hoffman BF (1978) Role of the sympathetic nervous system in arrhythmias occurring after coronary artery occlusion and myocardial infarction. In: Neural mechanisms in cardiac arrhythmias, p 115. Ed: Schwartz PJ, Brown AM, Malliani A, Zanchetti A. Raven Press, New York Lown B, Verrier RL, Rabinowitz SH (1977) Neural and psychologic mechanisms and the problem of sudden cardiac death. Am J Cardiol 39:890–902 Merx W, Yoon MS, Han J (1977) The role of local disparity on conduction and recovery on ventricular vulnerability to fibrillation. Am Heart J 94:603–610 Opie L, Owen P, Thomas W, Samson R (1973) Coronary sinus lactate measurements in assessment of myocardial ischemia. Am J Cardiol 32:295–305 Pappano AJ (1970) Calcium-dependent action potentials produced by catecholamines in guinea pig atrial muscle fibers depolarized by potassium. Circ Res 27:379–390 Sasynuik BI, Mendez C (1971) A mechanism for reentry in canine ventricular tissue. Circ Res 28:3–15 Schömig A, Dietz R, Strasser R, Kübler W (1981) Noradrenaline metabolism during myocardial ischemia. J Mol Cell Cardiol 13 (Suppl 1), 85 Senges J, Brachmann J, Pelzer D, Mizutani T, Kübler W (1979) Effects of some components of ischemia on electrical activity and reentry in the canine ventricular conducting system. Circ Res 44:864–872 Trautwein W, Gottstein U, Dudel J (1954) Der Aktionsstrom der Myokardfaser im Saucrstoffmangel. Pflügers Arch 260:40–60 Trautwein W, Schmidt RF (1960) Zur Membranwirkung des Adrenalins an der Herzmuskelfaser. Pflügers Arch 271:715–726 Vassalle M, Branabel O (1971) Norepinephrine and potassium fluxes in cardiac fibers. Pflügers Arch 322:287–303 Wellens AJJ, Lie KI, Durrer D (1974) Further observations on ventricular tachycardia as studied by electrical stimulation of the heart: Chronic recurrent ventricular tachycardia and ventricular tachycardia during acute myocardial infarction. Circulation 49:647–653 Wit AL, Hoffman BF, Cranefield PF (1972a) Slow conduction and reentry in the ventricular conducting system. I. Return extrasystole in canine Purkinje fibers. Circ Res 30:1–10 Wit AL, Cranefield PF, Hoffman BF (1972b) Slow conduction and reentry in the ventricular conducting system: II. Single and sustained circus movement in networks of canine and bovine Purkinje fibers. Circ Res 30:11–22 Wit AL, Bigger JT (1975) Possible electrophysiological mechanisms for lethal arrhythmias accompanying myocardial ischemia and infarction. Circulation 51/52 (Suppl III), 96–115