SUMMARYTo obtain information conceming the time course and instantaneous distribution of the excitatory process of the normal human healt, studies were made on isolated human hearts from seven individuals who died from various cerebral conditions, but who had no history of cardiac disease. Measurements were made from as many as 870 intramural terminals.In the isolated human hearts three endocardial areas were synchronously excited o to 5 msec after the start of the left ventricular activity potential. These areas increased rapidly in si ze dUl'ing the next 5 to 10 msec and became confluent in 15 to 20 msec. The left ventricular areas Rrst excited were (1) high on the anterior paraseptal wall just below the attachment of the mitral valve; (2) central on the left surface of the interventricular septum and (3) posterior paraseptal about one third of the distance from apex to base. The last part of the left ventricle to be activated usually was the posterobasal area. Endocardial activation of the right ventricle was found to start ne ar the insertion of the anterior papillary muscle 5 to 10 msec af ter onset of the left ventricular cavity potential. Septal activation started in the micldle third of the left side of the interventricular septurn, somewhat anteriorly, and at the lower third at the junction of the septum and posterior wall. The epicardial excitation pattem reflected the movements of the intramural excitation wave. Conduction velo city was determined in one heart by an appropriate stimulation technic. Atrial excitation, explored in two hearts, spread more or less according to concentric isochronic lines. Control studies, carried out on Rve canine hearts, disclosed that the pattem of ventricular excitation did not change af ter isolation and perfusion. However, total excitation was completed earlier in the isolated heart, and conduction velo city increased.Careful mapping illustrations are presented.Additional Indexing W ords:Ventricular excitation Intramural conduction velo city Epicardial excitation Atrial excitation K NOWLEDGE of the time course and instantaneous distribution of the excitatory pro ce ss of the normal human heart would be of value for an understanding of the QRS complex.Studies of this process during surgical intervention for heart disease or pulmonary

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Subepicardial transmembrane potentials were recorded from intact pig hearts to observe the changes induced by acute ischemia. Ischemia shortened action potential duration, and decreased its amplitude, upstroke velocity, and resting potential. The cells were unresponsive after 12 to 15 minutes of coronary artery occlusion, yet near normal action potentials could be restored by flushing the occluded artery with saline as late as 40 minutes after occlusion. The unipolar extracellular electrogram reflected unresponsiveness by a monophasic potential. Local refractory periods initially shortened by up to 100 msec. Later, postrepolarization refractoriness occurred and refractory periods lengthened often in excess of basic cycle length, thus resulting in 2:1 responses. The onset of early ventricular arrhythmias often coincided with a period of alternation and 2:1 responses, especially when these got out of phase in different regions. Reperfusion frequently led to ventricular fibrillation, and was associated with marked inhomogeneity in cellular responses. Re-entry within ischemic myocardium was the most likely mechanism for arrhythmias.

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SUMMARY We divised a method to determine tissue osmolality in intact beating hearts. After occlusion of the left anterior descending coronary artery (LAD) of isolated porcine hearts, tissue osmolality in the ischemic myocardium increased within 50 minutes by about 40 mOsm/kg. This rise in osmolality could be accounted for by metabolic processes, notably the conversion of glycogen into lactate, and the hydrolysis of high energy phosphates. Concomitant with the rise in osmolality, the ischemic myocardium during the 1-hour period of LAD occlusion took up fluid and increased tistue water volume by an average of 16.5%. We demonstrated that the osmolality of fixatives used for morphological studies markedly influences ischemic cell morphology. Thus, normotonic fixation of the ischemic myocardium accentuates cell swelling, whereas nearly normal cell volumes result from hypertonic fixation, adjusted according to the rise hi ischemic tissue osmolality. Normotonic reperfusion of the ischemic area after 1 hour of LAD occlusion resulted in the "no-refiow" phenomenon in the mldmural and subendocardial regions. Epicardial and intramural DC-electrograms showed persistent ischemic changes, i.e., T-Q depression, S-T elevation, and monophasic potentials. Tissue resistivity, which during ischemia had risen twofold, remained high. Lacate levels remained high, creatinephosphate (CP) and adenosinetriphosphate (ATP) levels remained low. Selective hypertonic reperfusion of the LAD, followed by a gradual return to normotonic perfnsion, resulted in a normalization of DC extracellular elcctrograms, restoration of electrical resistivity to near normal, low levels of lactate, and higher levels of CP and ATP although control values were not reached. Cell morphology was correspondingly normalized following this procedure. We conclude that ischemic cells become hyperosmotic and consequently take up additional fluid when exposed to normotonic blood. This increased cell swelling compresses capillaries, prevents reperfusion, and may be a major factor in causing reperfusion damage. This damage can be prevented to a large extent by selective hypertonic reperfusion. Circ Res 49: 364-381, 1881