Electrophysiology and electrocardiology of acute myocardial ischemia.
Transmembrane potentials and local direct current extracellular electrograms were simultaneously recorded from intact, isolated porcine and canine hearts, perfused according to the Langendorff technique with a 1:1 mixture of blood and Tyrode solution. Regional ischemia was produced by clamping the left anterior descending coronary artery. The first change produced by ischemia was a loss of resting membrane potential, resulting in a depression of the TQ-segment in the local electrogram. Later, action potential amplitude decreased, leading to true ST-segment elevation. Action potential shortening of ischemic cells caused positive T waves, provided activation delay was not marked. When activation of ischemic cells was considerably delayed, and repolarization in the ischemic area occurred later than in non-ischemic myocardium, local T waves became negative. Changes in TQ- and ST-segments and in T waves of local electrograms can qualitatively be explained by local current circuits, resulting from intracellular potential differences between ischemic and normal cells in the different phases of the cardiac cycle. ST-segment elevation, as recorded with conventional, condenser-coupled, alternating current amplifiers, can be caused by a diastolic current of injury (due to depolarization of resting membrane potential), or to a combination of diastolic and systolic current of injury (due to a reduction of action potential amplitude).
D000787:Angina Pectoris / Q000503:physiopathology; D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology*; D003971:Diastole; D004285:Dogs; D004562:Electrocardiography; D004594:Electrophysiology; D006321:Heart / Q000502:physiology* / Q000503:physiopathology; D006801:Humans; D008564:Membrane Potentials; D013552:Swine; D013599:Systole