Distribution of extracellular potassium and its relation to electrophysiologic changes during acute myocardial ischemia in the isolated perfused porcine heart.

An experimental approach is described to quantitate inhomogeneity in extracellular K concentration ([K+]out) in the presence of ischemia and to relate this inhomogeneity to the electrophysiologic changes. Extracellular potassium concentration and local direct-current electrograms from the same sites were measured in isolated perfused pig hearts with the use of multiple electrodes. Dispersion of [K+]out is described under three conditions: (1) during regional ischemia in the "central zone" and the "borderzone", (2) during global ischemia, and (3) during perfusion of the heart with a high-K perfusate. Inhomogeneity was greatest during regional ischemia, especially in the borderzone, where generally lower concentrations were measured. When during regional ischemia the normal zone was perfused with a high-K perfusate, dispersion in the ischemic borderzone diminished, and higher concentrations than in the central zone were measured. During global ischemia inhomogeneity was slightly larger than during high-K perfusion. Dispersion during the latter was considered due to experimental error. A decrease in [K+]out during regional ischemia after the initial increase was closely correlated with electrical recovery of the electrograms. This decrease occurred earlier in the borderzone than in the central zone. During ischemia [K+]out was not related to the occurrence of monophasic electrograms, which are indicative of the absence of local regenerative responses. For every single electrode position a linear relationship between TQ depression and [K+]out was found, the slope of which varied with the position of the electrode. When all sites were taken together, there was no correlation between TQ depression and [K+]out. We conclude that: (1) inhomogeneity of K+ is largest in the borderzone, (2) potassium flows from the ischemic zone into the normal zone, (3) transient electrical recovery is related to a decrease (after an initial increase) in [K+]out, which is at least partly due to a flow of K+ toward the normal zone, (4) monophasic ("block") electrograms can be recorded from intrinsically excitable tissue, (5) for every single site in the ischemic region there is a linear relationship between local [K+]out and local TQ segment depression, and (6) the degree of TQ depression at a particular site is not a reliable index of the degree of ischemic injury at that site.

[1]  J. L. Hill,et al.  Flexible valinomycin electrodes for on-line determination of intravascular and myocardial K+. , 1978, The American journal of physiology.

[2]  J. L. Hill,et al.  Factors related to vulnerability to arrhythmias in acute myocardial infarction. , 1982, American Heart Journal.

[3]  P. Schwartz,et al.  Effects of unilateral stellate ganglion stimulation and ablation on electrophysiologic changes induced by acute myocardial ischemia in dogs. , 1985, Circulation.

[4]  R. Patterson,et al.  Analysis of coronary collateral structure, function, and ischemic border zones in pigs. , 1983, The American journal of physiology.

[5]  S. Kimura,et al.  Intracellular K+ and Na+ activities under hypoxia, acidosis, and no glucose in dog hearts. , 1985, The American journal of physiology.

[6]  A. Kleber Extracellular potassium accumulation in acute myocardial ischemia. , 1984, Journal of molecular and cellular cardiology.

[7]  C Antzelevitch,et al.  Electrotonically Mediated Delayed Conduction and Reentry in Relation to “Slow Responses” in Mammalian Ventricular Conducting Tissue , 1981, Circulation research.

[8]  J. Kupersmith,et al.  Activity-dependent extracellular K+ fluctuations in canine Purkinje fibres , 1980, Nature.

[9]  R. Jennings,et al.  Studies on distribution and localization to potassium in early myocardial ischemic injury. , 1957, A.M.A. archives of pathology.

[10]  K. Shine,et al.  Extracellular potassium accumulation during myocardial ischemia: implications for arrhythmogenesis. , 1981, Journal of molecular and cellular cardiology.

[11]  M. Janse,et al.  Effect of changes in perfusion pressure on the position of the electrophysiologic border zone in acute regional ischemia in isolated perfused dog and pig hearts. , 1982, The American journal of cardiology.

[12]  J W Fiolet,et al.  Transmural inhomogeneity of energy metabolism during acute global ischemia in the isolated rat heart: dependence on environmental conditions. , 1985, Journal of molecular and cellular cardiology.

[13]  G. Moe,et al.  Nonuniform Recovery of Excitability in Ventricular Muscle , 1964, Circulation research.

[14]  A. Capucci,et al.  Variability of recovery of excitability in the normal canine and the ischaemic porcine heart. , 1985, European heart journal.

[15]  D. Zipes,et al.  Alterations in Canine Myocardial Excitability during Ischemia , 1977, Circulation research.

[16]  D Durrer,et al.  Mechanism and Time Course of S‐T and T‐Q Segment Changes during Acute Regional Myocardial Ischemia in the Pig Heart Determined by Extracellular and Intracellular Recordings , 1978, Circulation research.

[17]  K I Shine,et al.  Extracellular K+ accumulation during myocardial ischemia in isolated rabbit heart. , 1982, The American journal of physiology.

[18]  R. Holland,et al.  Precordial and Epicardial Surface Potentials during Myocardial Ischemia in the Pig: A THEORETICAL AND EXPERIMENTAL ANALYSIS OF THE TQ AND ST SEGMENTS , 1975, Circulation research.

[19]  A. Capucci,et al.  Electrophysiological basis for arrhythmias caused by acute ischemia. Role of the subendocardium. , 1986, Journal of molecular and cellular cardiology.

[20]  M J Janse,et al.  Electrotonic Interactions across an Inexcitable Region as a Cause of Ectopic Activity in Acute Regional Myocardial Ischemia: A Study in Intact Porcine and Canine Hearts and Computer Models , 1982, Circulation research.

[21]  G. R. Mines On dynamic equilibrium in the heart , 1913, The Journal of physiology.

[22]  J. Kupersmith,et al.  Spatial distribution of [14C]-lidocaine and blood flow in transmural and lateral border zones of ischemic canine myocardium. , 1982, The American journal of cardiology.

[23]  J. L. Hill,et al.  Interaction of Acidosis and Increased Extracellular Potassium on Action Potential Characteristics and Conduction in Guinea Pig Ventricular Muscle , 1982, Circulation research.

[24]  D. Durrer,et al.  The Effect of Acute Coronary Artery Occlusion on Subepicardial Transmembrane Potentials in the Intact Porcine Heart , 1977, Circulation.

[25]  A. Noma,et al.  ATP-regulated K+ channels in cardiac muscle , 1983, Nature.

[26]  D. Yellon,et al.  The "border zone" in evolving myocardial infarction: controversy or confusion? , 1981, The American journal of cardiology.

[27]  L. Clerc Directional differences of impulse spread in trabecular muscle from mammalian heart. , 1976, The Journal of physiology.

[28]  R. Coronel,et al.  The change of the free energy of ATP hydrolysis during global ischemia and anoxia in the rat heart. Its possible role in the regulation of transsarcolemmal sodium and potassium gradients. , 1984, Journal of molecular and cellular cardiology.

[29]  A. Kleber,et al.  The “Border Zone” in Myocardial Ischemia: An Electrophysiological, Metabolic, and Histochemical Correlation in the Pig Heart , 1979, Circulation research.

[30]  V. Wiegand,et al.  Extracellular potassium activity changes in the canine myocardium after acute coronary occlusion and the influence of beta-blockade. , 1979, Cardiovascular research.

[31]  R. Holland,et al.  TQ-ST segment mapping: critical review and analysis of current concepts. , 1977, The American journal of cardiology.

[32]  A. S. Harris Potassium and experimental coronary occlusion. , 1966, American heart journal.

[33]  A. Kléber,et al.  Resting Membrane Potential, Extracellular Potassium Activity, and Intracellular Sodium Activity during Acute Global Ischemia in Isolated Perfused Guinea Pig Hearts , 1983, Circulation research.

[34]  J. Brigham,et al.  Excitatory factors in ventricular tachycardia resulting from myocardial ischemia; potassium a major excitant. , 1954, Science.

[35]  D. Russell,et al.  Ventricular refractoriness during acute myocardial ischaemia and its relationship to ventricular fibrillation. , 1978, Cardiovascular research.

[36]  J. L. Hill,et al.  Effect of Acute Coronary Artery Occlusion on Local Myocardial Extracellular K+ Activity in Swine , 1980, Circulation.

[37]  S. Weidmann,et al.  The effect of the cardiac membrane potential on the rapid availability of the sodium‐carrying system , 1955, The Journal of physiology.

[38]  J Tranum-Jensen,et al.  The subendocardial border zone during acute ischemia of the rabbit heart: an electrophysiologic, metabolic, and morphologic correlative study. , 1986, Circulation.

[39]  G. Cherry,et al.  The relationship to ventricular fibrillation of early tissue sodium and potassium shifts and coronary vein potassium levels in experimental myocardial infarction. , 1971, The Journal of thoracic and cardiovascular surgery.

[40]  H. Walfridsson,et al.  Myocardial oxygen pressure across the lateral border zone after acute coronary occlusion in the pig heart. , 1985, Advances in experimental medicine and biology.

[41]  P. Corr,et al.  Amphipathic metabolites and membrane dysfunction in ischemic myocardium. , 1984, Circulation research.