Time course of changes in intracellular K+, Na+, and pH of subendocardial Purkinje cells during the first 24 hours after coronary occlusion.

Abstract

We investigated the basis for the alterations in the intracellular potassium and sodium activity occurring in subendocardial Purkinje fibers surviving in 24-hour infarcts by examining ion activities in these Purkinje fibers removed from infarcting hearts at earlier times. Specifically, we examined intracellular potassium activity, sodium activity, and pH at 1 and 3 hours after ligation of the left anterior descending coronary artery, and we correlated the changes in ion activity with changes in maximum diastolic potential. We tested various mechanistic hypotheses relating to how the ion activity changes develop and how they affect membrane potential. We We also reported that intracellular Na+ activity (aNa1) was elevated in the Purkinje fibers surviving in infarcted hearts 24 hours after ligation. However, the aNal elevation was only a small portion (approximately 10%) of the aKi reduction. The aNai elevation suggests possible suppression of the Na,K-ATPase pump. However, because the reduction in aKi greatly exceeds the increase in aNai, pump suppression alone is probably not the sole mechanism of the K' loss.7 Consistent with these findings is a second possible mechanism for the loss of K', that is, that intracellular acidification leads to an increase in mobile anions that accompany the K' efflux.58-10 However, we were unable to find any evidence for acidification by measuring pHi in Purkinje fibers at 24 hours, and in fact pHi was slightly basic at that time.6These findings have caused us to consider two mechanistic questions regarding membrane depolarization of the subendocardial Purkinje fibers from 24-hour-old infarcts: 1) What factors are responsible for aKi reduction and aNai elevation? 2) What factors besides EK

Triggered activity due to delayed afterdepolarizations in sites of focal origin of ischemic ventricular tachycardia

“…In the latter, fibers were removed from visibly infarcted myocardium with minimal or no mapping (4,6,13,14,16,17,19). In vivo and in vitro correlation studies showed that spontaneous VT originates in Purkinje tissue.…”

“…In coronary sinus, mitral valve, and some atrial preparations, catecholamines may also produce TA (32). Ischemia serves as a typical model as well, because the acute process produces intracellular Ca 2ϩ (18) as well as Na ϩ (14) overload. The addition of catecholamines may also facilitate TA but is not required.…”

Differential Effects of a Segment of Slow Conduction on Reentrant Ventricular Tachycardia in the Rabbit Heart

“…In acute ischemia, the elevated extracellular potassium is only one of the factors that depress the active membrane properties, and other changes in ionic composition and metabolic compounds are involved as well. [11][12][13][14][15] An important limitation of the present model is that we have deliberately reduced the ventricles to a 2-dimensional subepicardial substrate of VT. Cryoablation of the endocardial and midmyocardial layers of the left ventricle eliminated the possible participation of these structures in our studies. This is in contrast to the arrhythmogenic substrate after chronic myocardial infarction, which has a more complex 3D architecture.…”

Flow cytometric determination of intracellular free potassium concentration

“…Fluorescent indicators have recently been developed to measure the intracellular free Ca 21 (41), Na 1 (17), and K 1 (22) concentrations. A remarkable amount of new information was gained by using fluorescent Ca 21 chelators. The impact of Na 1 and K 1 indicators is significantly less because of their limited specificity.…”